genename	geneid	genetype	pmid	year	reference	disease	description	direction	tissues_cells	species	rowid
HOXA11	ENSG00000005073	lncRNA	31757938	2019	Silencing of long noncoding RNA HOXA11-AS inhibits the Wnt signaling pathway via the upregulation of HOXA11 and thereby inhibits the proliferation, invasion, and self-renewal of hepatocellular carcinoma stem cells	hepatocellular carcinoma (HCC)	The results revealed that HOXA11 overexpression reduced the number of tumorspheres, cell colonies, invaded cells and proliferative cells. HOXA11-AS silencing exerts an antitumor effect, suppressing HCC development via Wnt signaling pathway inactivation by decreasing the methylation level of the HOXA12 promoter.	Downregulation	Hep3B, Huh7	Human	117
TCF7	ENSG00000081059	lncRNA	34868900	2021	LncRNA TCF7 Promotes Epithelial Ovarian Cancer Viability, Mobility and Stemness via Regulating ITGB8	epithelial ovarian cancer (EOC)	Lnc-TCF7 was upregulated in EOC cell lines. Lnc-TCF7 regulates multiple oncogenic pathways, promotes proliferation, migration, invasion, stemness via upregulating ITGB8. Lnc-TCF7 overexpression promoted CD44 expression, CD133 expression, CD44+CD133+ cell proportion, sphere formation ability, while decreased cisplatin sensitivity in SKOV3 cells.	Upregulation	SKOV3	Human	625
TPTEP1	ENSG00000100181	lncRNA	33173989	2020	lncRNA TPTEP1 inhibits stemness and radioresistance of glioma through miR-106a-5p-mediated P38 MAPK signaling	glioma	TPTEP1 attenuated stemness and radioresistance of glioma both in vitro and in vivo.TPTEP1 augmented MAPK14 expression by competitively interacting with miR-106a-5p, thus activating the P38 MAPK signaling pathway, and suppressing glioma stemness and radioresistance. Low TPTEP2 expression levels were detected in high-grade glioma tissues compared with low-grade glioma tissues.	Upregulation	SHG44, U-251MG	Human	637
RP1	ENSG00000104237	lncRNA	31073122	2019	KLF5 regulated lncRNA RP1 promotes the growth and metastasis of breast cancer via repressing p27kip1 translation	breast cancer (BRCA)	RP1 was highly expressed in breast cancer and predicted poor prognosis of breast cancer patients. RP1 promotes proliferation, invasion, and stemness of breast cancer cells via p27kip1. RP1 promoted the proliferation and metastasis of breast cancer cells in vitro and in vivo. RP1 maintained the EMT and stemness states of breast cancer cells via repressing p27kip1 protein expression.	Upregulation	MDA-MB-231, BT549	Human	601
LINC00525	ENSG00000146666	lncRNA	31242722	2019	Long Non-Coding RNA LINC00525 Promotes the Stemness and Chemoresistance of Colorectal Cancer by Targeting miR-507 or ELK3 Axis	colorectal carcinoma (CRC)	Interestingly, LINC-00525 expression levels were significantly increased in sphere-forming HTC116 and HT29 cells when compared with those in the parent cells. The results also demonstrated that LINC00525 knockdown significantly decreased the capacity to form tumorsphere when compared with those in the control group. LINC00525 enhanced stemness properties and increased sensitivities of CRC cells to oxaliplatin by targeting miR-507 or ELK3 axis	Upregulation	HCT116, HT29	Human	148
TALNEC2	ENSG00000163364	lncRNA	28423669	2017	The novel long non-coding RNA TALNEC2, regulates tumor cell growth and the stemness and radiation response of glioma stem cells	glioblastoma (GBM)	TALNEC2 was highly expressed in GBM with poor prognosis, in GBM specimens derived from short-term survivors and in glioma cells and glioma stem cells (GSCs). The expression of TALNEC2 is associated with the increased tumorigenic potential of GSCs and their resistance to radiation. We found that silencing of TALNEC2 in the HF2355 and HF2414 GSCs decreased the self-renewal and the frequency of sphere formation.	Upregulation	A172, U87, MCF-7	Human	624
TPT1-AS1	ENSG00000170919	lncRNA	35022996	2022	Long Non-coding RNA TPT1-AS1 Suppresses APC Transcription in a STAT1-Dependent Manner to Increase the Stemness of Colorectal Cancer Stem Cells	colorectal carcinoma (CRC)	TPT1-AS1 was identified as a significantly upregulated gene in CRC. TPT1-AS1 was significantly highly expressed in the CSCs compared to non-stem cells. TPT1-AS1 recruits STAT1 to suppress APC transcription and increase the stemness of colorectal CSCs via Wnt or beta-catenin activation.	Upregulation	HCT116, CACO2	Human	636
SNHG11	ENSG00000174365	lncRNA	33068778	2021	lncRNA SNHG11 Promotes Gastric Cancer Progression by Activating the Wnt or beta-Catenin Pathway and Oncogenic Autophagy	gastric cancer (GC)	SNHG11 is upregulated in GC, and that its upregulation correlated with dismal patient outcomes. As expected, knockdown of SNHG11 impeded the sphere formation capacity of GC cells. SNHG11 aggravated oncogenic autophagy to facilitate cell proliferation, stemness, migration, invasion, and epithelial-to-mesenchymal transition (EMT) in GC.	Upregulation	SGC-7901, MKN-45	Human	606
LINC01106	ENSG00000175772	lncRNA	33067422	2020	LINC01106 drives colorectal cancer growth and stemness through a positive feedback loop to regulate the Gli family factors	colon adenocarcinoma (COAD)	LINC01106 was expressed higher in CRC cells than that in normal cells. Sphere formation of CRC cells was attenuated by the knockdown of LINC01106. LINC01106 induced the proliferation, migration, and stem-like phenotype of CRC cells. Gli2-induced upregulation of LINC01106 aggravates CRC progression through upregulating Gli2, Gli2, and Gli4.	Upregulation	LoVo, SW1116	Human	158
LINC00324	ENSG00000178977	lncRNA	32128906	2020	Long noncoding RNA LINC00324 exerts protumorigenic effects on liver cancer stem cells by upregulating fas ligand via PU box binding protein	liver cancer (HULC)	LINC00324 was highly expressed in LCSCs. Silencing of LINC00324 or FasL suppressed expression of stemness-related genes, cell viability, proliferation, migration, invasion, self-renewal, and tumorigenesis, but enhanced cell apoptosis. LINC00324 silencing significantly reduced the self-renewal ability of the HuH-7 stem cells by inhibiting the sphere formation.	Upregulation	HuH-7	Human	143
LINC01559	ENSG00000180861	lncRNA	32895368	2020	Exosome-transferred LINC01559 promotes the progression of gastric cancer via PI3K or AKT signaling pathway	gastric cancer (GC)	LINC01559 was upregulated in GC tissues. Likewise, the migratory ability and sphere formation efficiency were both enhanced by upregulation of LINC01559. In vitro experiments revealed that silencing LINC01559 remarkably hindered GC cell proliferation, migration and stemness. LINC01559 targeted both PGK1 and PTEN to promote GC progression by activating PI3K or AKT pathway.	Upregulation	HGC-27, AGS	Human	165
WT1-AS	ENSG00000183242	lncRNA	32349718	2020	LncRNA WT1-AS over-expression inhibits non-small cell lung cancer cell stemness by down-regulating TGF-beta1	non-small cell lung cancer (NSCLC)	We found that WT1-AS was down-regulated, while TGF-beta1 was upregulated in NSCLC tissues. WT1-AS over-expression may inhibit non-small cell lung cancer cell stemness by down-regulating TGF-beta1.	Downregulation	NCI-H522, NCI-H23	Human	641
GATA3-AS1	ENSG00000197308	lncRNA	33760161	2021	LncRNA GATA3-AS1-miR-30b-5p-Tex10 axis modulates tumorigenesis in pancreatic cancer	pancreatic cancer (PaCa)	Upregulation of GATA3-AS1 was revealed in PC tissues and cell lines. Knockdown of GATA3-AS1 in PANC-1 or AsPC-1 cells markedly reduced cell viability, cell proliferation, and cell invasion abilities. In addition, GATA3-AS1 knockdown suppressed the stemness of PANC-1 and AsPC-1 cells by decreasing the spheroid formation ability. GATA3-AS1-miR-30b-5p-Tex10 axis modulates tumorigenesis in PC, which may be associated with the Wnt or beta-catenin signaling pathway.	Upregulation	PANC-1, AsPC-1	Human	92
SNHG12	ENSG00000197989	lncRNA	36183925	2022	Identification of stemness index-related long noncoding RNA SNHG12 in human bladder cancer based on WGCNA	bladder cancer (BLCA)	SNHG12 was high expression in both bladder cancer tissues and cells. SNHG12 promoted proliferation, invasion, migration, apoptosis and stemness of bladder cancer cells in vitro and tumour proliferation in vivo.	Upregulation	T24, UMUC-3	Human	607
SNHG12	ENSG00000197989	lncRNA	32239639	2020	Long noncoding RNA SNHG12 induces proliferation, migration, epithelial-mesenchymal transition, and stemness of esophageal squamous cell carcinoma cells via post-transcriptional regulation of BMI1 and CTNNB1	esophageal squamous cell carcinoma (ESCC)	SNHG12 mainly distributed in ESCC cell cytoplasm, was overexpressed in ESCC specimens and CD133+ cells. SNHG12 induces proliferation, migration, EMT, and stemness of ESCC cells via post-transcriptional regulation of BMI1 and CTNNB1.	Upregulation	EC9706, EC109, KYSE410, KYSE150, KYSE450	Human	608
SNHG12	ENSG00000197989	lncRNA	34096799	2021	Long Noncoding RNAs for Predicting Prognosis of Patients with Hepatocellular Carcinoma	hepatocellular carcinoma (HCC)	Functional studies on SNHG12, the leading candidate of the risk lncRNAs, revealed that knockdown of SNHG12 reduces the abilities of HCC cells stemness, proliferation, migration, and invasion.	Upregulation	HepG2, HCCLM3	Human	609
TDRG1	ENSG00000204091	lncRNA	35730470	2022	Long non-coding RNA TDRG1 aggravates colorectal cancer stemness by binding with miR-873-5p to upregulate PRKAR2	colorectal carcinoma (CRC)	TDRG1 level was upregulated in CRC cells compared to that in normal colon epithelial cells. Additionally, TDRG1 level was remarkably upregulated in 3D non-adherent spheres derived from the parental CRC cells. Further in vitro and in vivo revealed that TDRG1 knockdown suppressed the stemness of CRC cells.	Upregulation	HT29, HCT-116	Human	626
TDRG1	ENSG00000204091	lncRNA	36444968	2022	Long non-coding RNA TDRG1 aggravates lung cancer stemness by binding to Sox2 mRNA	non-small cell lung cancer (NSCLC)	It was found that TDRG1 was highly expressed in NSCLC cells relative to that in normal lung epithelial cells. LncRNA TDRG1 exhibits a higher level in spheres derived from NSCLC cells and aggravates NSCLC cell stemness in vitro. LncRNA TDRG1 facilitates NSCLC stemness by directly binding to and enhancing the stability of Sox2 mRNA.	Upregulation	A549, H1975	Human	627
ZNF204P	ENSG00000204789	lncRNA	35168700	2022	ZNF204P is a stemness-associated oncogenic long non-coding RNA in hepatocellular carcinoma	hepatocellular carcinoma (HCC)	We found that ZNF204P is up-regulated in tumor samples with poor prognosis. ZNF204P knockdown impairs cell proliferation and migration or invasion. ZNF204P promotes tumorigenesis through the miRNA-145-5p or OCT4, SOX2 axis.	Upregulation	HepG2	Human	645
FAM83A-AS1	ENSG00000204949	lncRNA	35002507	2022	LncRNA FAM83A-AS1 facilitates tumor proliferation and the migration via the HIF-1alpha or glycolysis axis in lung adenocarcinoma	lung adenocarcinoma (LUAD)	FAM83A-AS1 could impact the cell stemness by influencing the expression of CD133, CD44, and ALDH1 in LUAD under hypoxic conditions. FAM83A-AS1 could promote the migration and invasion of LUAD cells, as well as influence the stemness of LUAD cells in vivo and vitro. FAM83A-AS1 contributes to LUAD proliferation and stemness via the HIF-1alpha or glycolysis axis	Upregulation	A549, H358	Human	78
HLA-F-AS1	ENSG00000206446	lncRNA	33618253	2021	STAT3-induced HLA-F-AS1 promotes cell proliferation and stemness characteristics in triple negative breast cancer cells by upregulating TRABD	triple negative breast cancer (TNBC)	HLA-F-AS1 expression was significantly upregulated in TNBC tissues and cells, and high level of HLA-F-AS1 indicated the poor prognosis of patients with TNBC. We carried out sphere formation assay. It was shown that HLA-F-AS1 deficiency reduced sphere diameter and number of spheres. STAT3-induced HLA-F-AS1 facilitates cell proliferation and stemness characteristics in TNBC by miR-541-3p-dependent upregulation of TRABD.	Upregulation	MDA-MB-231, MDA-MB-468	Human	105
SNORA42	ENSG00000207475	snoRNA	24886050	2014	Small nucleolar RNA signatures of lung tumor-initiating cells	non-small cell lung cancer (NSCLC)	Functional analysis indicated that snoRA42 was upregulated in CD133+ cells isolated from NSCLC cell lines compared with the CD133- counterparts. SnoRA42 knockdown reduced the proliferation and self-renewal of TICs in vitro. Ectopic expression of snoRA42 in non-TICs enhanced the potentials of cell proliferation and self-renewal. Blocking snoRA42 expression in TIC xenografts decreased tumorigenesis in mice.	Upregulation	H-1944, Calu-1	Human	613
SNORD89	ENSG00000212283	snoRNA	31395064	2019	SNORD89 promotes stemness phenotype of ovarian cancer cells by regulating Notch1-c-Myc pathway	ovarian cancer (OC)	SNORD89 highly expressed in ovarian cancer stem cells. The overexpression of SNORD89 resulted in the increased stemness markers, S phase cell cycle, cell proliferation, invasion and migration ability in OV and CA cells. SNORD89 deteriorates the prognosis of ovarian cancer patients by regulating Notch1-c-Myc pathway to promote cell stemness and acts as an oncogene in ovarian tumorigenesis.	Upregulation	OVCAR-3, CAOV-3	Human	615
SRA	ENSG00000213523	lncRNA	33000206	2020	Steroid receptor RNA activator inhibits the migration, invasion and stemness characteristics of renal cell carcinoma cells	renal cell carcinoma (RCC)	The decreased expression level of SRA was first confirmed in RCC tissues and cell lines by RT-qPCR. SRA is an important molecule that inhibits the migration, invasion and stem cell characteristics of RCC cells. The present study found that the overexpression of SRA reduced the sphere-forming effi-ciency of A498 cells , while the knockdown of SRA induced SKRC39 cell to form spheres.	Downregulation	SKRC39, A498	Human	622
UCA1	ENSG00000214049	lncRNA	30410864	2018	LncRNA UCA1 is necessary for TGF-beta-induced epithelial-mesenchymal transition and stemness via acting as a ceRNA for Slug in glioma cells	glioma	The expression of UCA1 is significantly increased by transforming growth factor-beta (TGF-beta) treatment in glioma cells and is greater in glioma tissues than in normal adjacent tissues. In addition, the enhancement of the stemness of glioma cells mediated by TGF-beta was abrogated by UCA1 knockdown, evident by the rescue of sphere formation. UCA1 may act as a ceRNA to promote Slug expression, which underlies TGF-beta-induced EMT and stemness of glioma cells.	Upregulation	U87, U251	Human	639
LINC00680	ENSG00000215190	lncRNA	33499874	2021	LINC00680 enhances hepatocellular carcinoma stemness behavior and chemoresistance by sponging miR-568 to upregulate AKT3	hepatocellular carcinoma (HCC)	LINC00680 was remarkably upregulated in HCC tissues. Suppression of LINC00680 significantly inhibited primary and secondary sphere formation capability of SNU-449 and SK-hep1 cell, whereas LINC00680 overexpression in Huh7 cells produced an opposite result. LINC00680 promotes HCC stemness properties and decreases chemosensitivity through sponging miR-568 to activate AKT3.	Upregulation	SNU-449, SK-hep1	Human	154
LINK-A	ENSG00000215808	lncRNA	32218837	2020	LINK-A lncRNA is upregulated in osteosarcoma and regulates migration, invasion and stemness of osteosarcoma cells	osteosarcoma (OS)	LINK-A is upregulated in osteosarcoma. Compared with the control groups, LINK-A lncRNA knockdown significantly inhibited, whereas treatment with TGF-beta1 at a dose of 10 ng or ml significantly promoted the migration, invasion and stemness (reflected by percentage of CD133+ cells) of cells of MG-63 and U2OS osteosarcoma cell lines.	Upregulation	MG-63, U2OS	Human	175
TINCR	ENSG00000223573	lncRNA	31540772	2019	Knockdown of long non-coding RNA TINCR decreases radioresistance in colorectal cancer cells	colorectal carcinoma (CRC)	Knockdown of TINCR suppresses the stemness of radioresistant SW620 cells. Knockdown of TINCR inhibited sphere formation ability in SW620R cells.	Upregulation	SW620, HTC116	Human	632
TINCR	ENSG00000223573	lncRNA	36385098	2022	The long noncoding RNA TINCR promotes self-renewal of human liver cancer stem cells through autophagy activation	hepatocellular carcinoma (HCC)	TINCR was found to be highly expressed in HCC tissues and LCSCs. Additionally, we observed the number of primary sphere and secondary sphere formation were reduced after TINCR knockdown. TINCR regulated LCSC self-renewal by autophagy activation through PTBP1 or ATG5 regulatory pathway.	Upregulation	HCCLM3, MHCC97L	Human	633
LINP1	ENSG00000223784	lncRNA	30416386	2018	TGF-beta or SMAD4-Regulated LncRNA-LINP1 Inhibits Epithelial-Mesenchymal Transition in Lung Cancer	lung cancer (LC)	As expected, inhibition of LINP1 significantly promoted sphere formation both in the number and the size. Conversely, when LINP1 was overexpressed in A549 cells, there was a significant decrease in cell migration, invasion, and sphere formation. LINP1 suppressed EMT of lung cancer cells, thereby controlling cancer cell migration, invasion, and stemless. Moreover, LINP1 inhibited TGF-beta-induced EMT and cell invasion in lung cancer cells.	Downregulation	A549	Human	176
HOXD-AS1	ENSG00000224189	lncRNA	32857725	2020	SP1-induced HOXD-AS1 promotes malignant progression of cholangiocarcinoma (CCA) by regulating miR-520c-3p or MYCN	cholangiocarcinoma (CCA)	HOXD-AS1 expression was significantly upregulated in CCA tissues and cells compared with control groups, respectively. Spheroid formation assays certified that HOXD-AS1 knockdown inhibited the formation of tumor spheroid in CCLP-1 cells, whereas HOXD-AS1 overexpression promoted the spheroid formation of CCA cells. HOXD-AS1 facilitated tumor proliferation, migration, invasion, EMT, stemness and drug resistance in vitro and in vivo. HOXD-AS1-induced malignant phenotypes were rescued by interfering miR-520c-3p and MYCN, respectively.	Upregulation	CCLP-1, QBC939	Human	125
LOCCS	ENSG00000224310	lncRNA	29110645	2017	Long intergenic non-protein-coding RNA 1567 (LINC01567) acts as a sponge against microRNA-93 in regulating the proliferation and tumorigenesis of human colon cancer (CC) stem cells	colon cancer (CC)	LOCCS, with obviously upregulated expression in colon CSCs. Knockdown of LOCCS reduced cell proliferation, invasion, migration, and generation of tumor xenografts.	Upregulation	SW1116	Human	190
DUXAP9	ENSG00000225210	lncRNA	34086387	2021	Long non-coding RNA DUXAP9 promotes hepatocellular carcinoma cell stemness via directly interacting with sox9	hepatocellular carcinoma (HCC)	DUXAP9 expression was recently found to be higher in hepatocellular carcinoma (HCC) tissues and cells, DUXAP9 positively regulated HCC cell stemness, as characterized by the change of sphere-formation ability, ALDH activity and stemness marker expression.The effects induced by DUXAP9 on HCC cell stemness depended on sox9 expression.	Upregulation	HepG2, Huh7	Human	75
PCAT3	ENSG00000225937	lncRNA	29552304	2018	The PCAT3 or PCAT9-miR-203-SNAI2 axis functions as a key mediator for prostate tumor growth and progression	prostate cancer (PCa)	Knockdown of PCAT3 and PCAT9 suppressed cellular proliferation, invasion, migration, angiogenesis and stemness in androgen-dependent LNCaP and 22Rv1 cells.Silence of miR-203 or ectopic expression of SNAI2 attenuated the inhibitory effect of PCAT3 and PCAT9 knockdown on cell proliferation and migration in vitro, and xenograft growth in vivo.	Upregulation	LNCaP, 22Rv1	Human	589
LAMP5-AS1	ENSG00000225988	lncRNA	32552847	2020	The lncRNA LAMP5-AS1 drives leukemia cell stemness by directly modulating DOT1L methyltransferase activity in MLL leukemia	mixed-lineage leukemia (MLL)	LAMP5-AS1 is specifically overexpressed in MLL leukemia patients (n = 58) than that in the MLL-wt leukemia (n = 163) (p<0.001). LAMP5-AS1 suppression significantly reduced colony formation and increased differentiation of primary MLL leukemia CD34+ cells.	Upregulation	MOLM13	Human	131
FGF13-AS1	ENSG00000226031	lncRNA	30771425	2019	Long non-coding RNA FGF13-AS1 inhibits glycolysis and stemness properties of breast cancer cells through FGF13-AS1 or IGF2BPs or Myc feedback loop	breast cancer (BRCA)	FGF13-AS1 expression is decreased in breast cancer tissue compared with corresponding normal tissue, and the downregulation of FGF13-AS1 is associated with poor prognosis. As expected, FGF13-AS1 transfection significantly limited the size and the number of spheroids derived from MDA-MB-231 cells. In contrast, knockdown of FGF13-AS1 increased the size and number of mammospheres derived from MCF-7 cells. FGF13-AS1 inhibits breast cancer cells proliferation, migration, and invasion by impairing glycolysis and stemness properties.	Downregulation	MCF-7, MDA-MB-231, MDA-MB-468, T47D	Human	83
SLC16A1-AS1	ENSG00000226419	lncRNA	32450050	2020	Long non-coding RNA SLC16A1-AS1: its multiple tumorigenesis features and regulatory role in cell cycle in oral squamous cell carcinoma	oral squamous cell carcinoma (OSCC)	SLC16A1-AS1 was significantly highly expressed in OSCC samples than that in normal samples. Silencing SLC16A1-AS1 significantly reduced the cell proliferation rate and colony-forming ability in both CAL27 and SCC25 cell lines.	Upregulation	SCC25, CAL27	Human	603
THOR	ENSG00000226856	lncRNA	32665537	2020	Long Non-Coding RNA THOR Enhances the Stem Cell-Like Traits of Triple-Negative Breast Cancer Cells Through Activating beta-Catenin Signaling	breast cancer (BRCA)	THOR was overexpressed in triple-negative breast cancer compared to that in luminal A- and B-type breast cancer. THOR silencing reduced TNBC cell stemness, which was evident by the decreased sphere-formation ability, stemness marker expression and ALDH1 activity.THOR facilitates TNBC cell stemness through activating -catenin signaling.	Upregulation	MDA-MB-453, MDA-MB-231	Human	628
THOR	ENSG00000226856	lncRNA	30227327	2018	LncRNA THOR increases the stemness of gastric cancer cells via enhancing SOX9 mRNA stability	gastric cancer (GC)	THOR level was significantly upregulated in gastric cancer tissues compared with that in normal adjacent tissues. Knockdown of THOR attenuated the stemnness of gastric cancer cells, evident by the decrease of stemness markers expression and capacity of cells spheroid formation. THOR could potentiate the stemness of gastric cancer cells via directly binding to SOX9 3'UTR.	Upregulation	BGC-823, MKN-45	Human	629
THOR	ENSG00000226856	lncRNA	29959065	2018	LncRNA THOR attenuates cisplatin sensitivity of nasopharyngeal carcinoma cells via enhancing cells stemness	nasopharyngeal carcinoma (NPC)	THOR was significantly increased in NPC tissues and non-adherent NPC spheres. Further in vitro and in vivo experiments were carried out and identified that knockdown of THOR attenuated NPC cells stemness, characterized as the decrease of spheres formation ability, cell proliferation, migration, invasion, stemness markers expression and tumor initiation, and enhanced cisplatin sensitivity of NPC cells.	Upregulation	HN4, FaDu	Human	630
THOR	ENSG00000226856	lncRNA	30984551	2019	LncRNA THOR increases osteosarcoma cell stemness and migration by enhancing SOX9 mRNA stability	osteosarcoma (OS)	The level of THOR is remarkably upregulated in OS cell spheroids compared to that in OS adherent cells. THOR overexpression increased spheroid formation ability and aldehyde dehydrogenase 1 (ALDH1) activity in OS adherent cells. THOR can promote the stemness and migration of OS cells by directly binding to the middle region of SOX9 3'UTR, thereby enhancing SOX9 mRNA stability and increasing its expression.	Upregulation	MG63	Human	631
ANCR	ENSG00000226950	lncRNA	34333213	2021	Long noncoding RNA ANCR promotes migration, invasion, EMT progress and stemness of nasopharyngeal carcinoma cells via the miR-4731-5p or NMT1 axis	nasopharyngeal carcinoma (NPC)	Then the expression of proteins related to cell stemness was also measured by the western blot. The levels of CD133, Oct4, Nanog were reduced by the transfection of si-ANCR_1 or 2 in NPC cells, which suggested that knockdown of ANCR decreased the cell stemness in NPC. Sphere formation assay was used to further determine the cell stemness in NPC, which showed that mammosphere numbers were reduced by the ANCR deficiency, which verified that ANCR enhanced the cancer stem cell (CSC) characteristics in NPC.	Upregulation	5-8F, C666-1	Human	6
DANCR	ENSG00000226950	lncRNA	31860165	2020	The long non-coding RNA DANCR regulates the inflammatory phenotype of breast cancer cells and promotes breast cancer progression via EZH2-dependent suppression of SOCS3 transcription	breast cancer (BRCA)	DANCR was significantly up-regulated in tissue samples from patients with breast cancer, as well as in breast cancer cell lines, as compared with normal tissues and breast epithelial cells, respectively. To investigate the impact of DANCR on CSC activity, we performed the mammosphere formation assay and found that shDANCR significantly reduced the size and number of mammospheres formed. The inhibition of targeting DANCR on self-renewal of CSCs was not limited to the first generation of mammospheres, but persisted till at least the 4th generation.	Upregulation	MDA-MB-231, MDA-MB-468	Human	62
DANCR	ENSG00000226950	lncRNA	25964079	2016	Long noncoding RNA DANCR increases stemness features of hepatocellular carcinoma by derepression of CTNNB1	hepatocellular carcinoma (HCC)	DANCR overexpression led to increased stemness features. The number,size and the sphere-initiating cell frequency of spheroids could be enhanced by enforced DANCR expression.	Upregulation	P213, P892, P893	Human	63
DANCR	ENSG00000226950	lncRNA	33302540	2020	Long Noncoding RNA DANCR Activates Wnt or beta-Catenin Signaling through MiR-216a Inhibition in Non-Small Cell Lung Cancer	non-small cell lung cancer (NSCLC)	DANCR knockdown (KD) impeded cell migration and reduced stem-like characteristics in two NSCLC cell lines, A549 and H1755. Stable KD of DANCR expression in A549 cells reduced the percentage of tumorspheres that formed without affecting tumorsphere size. DANCR KD reduced beta-catenin signaling and protein expression, and decreased the expression of beta-catenin gene targets c-Myc and Axin2.	Upregulation	A549, H1755	Human	64
DANCR	ENSG00000226950	lncRNA	28642170	2017	lncRNA DANCR promotes tumor progression and cancer stemness features in osteosarcoma by upregulating AXL via miR-33a-5p inhibition	osteosarcoma (OS)	Furthermore, sphere formation assays showed that DANCR knockdown strongly suppressed sphere formation capacities, whereas DANCR over-expression significantly increased sphere numbers and sizes in both 143B and HOS cells.Over-expression of the lncRNA DANCR increased osteosarcoma cell proliferation, migration, and invasion in vitro, as well as promoted xenograft tumor growth and lung metastasis in vivo. DANCR increases CSCs function by upregulating AXL via competitively binding to miR-33a-5p, and this function is sequentially performed through the PI3K-Akt signaling pathway.	Upregulation	HOS, 143B	Human	65
DANCR	ENSG00000226950	lncRNA	31804607	2020	IGF2BP2 regulates DANCR by serving as an N6-methyladenosine reader	pancreatic cancer (PaCa)	Ectopic expression of DANCR in BXPC-3 and SW1990 cells increased the sphere formation, spheres derived from DANCR overexpression were not only larger in size, but also the number of spheres was more than vector control cells. DANCR promotes cell proliferation and stemness-like properties. Experiments with xenograft models revealed that while ectopic expression of DANCR promotes, DANCR KO suppresses tumor growth.	Upregulation	BXPC-3, SW1990	Human	66
LINC00511	ENSG00000227036	lncRNA	30482236	2018	Long noncoding RNA LINC00511 contributes to breast cancer tumourigenesis and stemness by inducing the miR-185-3p or E2F1 or Nanog axis	breast cancer (BRCA)	LINC00511 was measured to be highly expressed in the breast cancer specimens and the high-expression was correlated with the poor prognosis. LINC00511 promoted the proliferation, sphere-formation ability, stem factors (Oct4, Nanog, SOX2) expression and tumor growth in breast cancer cells. LINC00511 or miR-185-3p or E2F1 or Nanog axis facilitates the breast cancer stemness and tumorigenesis.	Upregulation	MDA-MB-231, MCF-7	Human	146
LINC00511	ENSG00000227036	lncRNA	34427967	2021	LINC00511 promotes gastric cancer progression by regulating SOX4 and epigenetically repressing PTEN to activate PI3K or AKT pathway	gastric cancer (GC)	LINC00511 was detected to be highly expressed in GC cells. Next, sphere formation assay was implemented and the results revealed that sphere formation efficiency was decreased after the transfection of sh-LINC00511 in GC cells. SOX4-induced LINC00511 activated SOX4 via competing endogenous RNA (ceRNA) pattern and epigenetically repressed PTEN to activate PI3K or AKT pathway by recruiting EZH2, thus facilitating GC cell proliferation, migration and stemness while inhibiting GC cell apoptosis.	Upregulation	HGC-27, SNU-1	Human	147
LINC01806	ENSG00000227403	lncRNA	35599309	2022	LINC01806 mediated by STAT1 promotes cell proliferation, migration, invasion, and stemness in non-small cell lung cancer through Notch signaling by miR-4428 or NOTCH2 axis	non-small cell lung cancer (NSCLC)	LINC01806 expression was high in NSCLC cell lines. Inhibition of LINC01806 attenuated cell stemness in NSCLC. The data from sphere formation assay also demonstrated that BEAS-2B cell stemness was enhanced by LINC01806 up-regulation. Likewise, we observed that the attenuated sphere-forming ability of NSCLC cells caused by LINC01806 depletion was enhanced upon miR-4428 down-regulation or NOTCH2 overexpression. LINC01806 knockdown impeded cell proliferation, migration, invasion, and stemness, along with tumor growth. LINC01806 enhanced NOTCH2 expression to stimulate Notch signaling via sponging miR-4428, thereby facilitating NSCLC progression.	Upregulation	H1650, H1299	Human	167
PCAT9	ENSG00000227418	lncRNA	29552304	2018	The PCAT3 or PCAT9-miR-203-SNAI2 axis functions as a key mediator for prostate tumor growth and progression	prostate cancer (PCa)	Knockdown of PCAT3 and PCAT9 suppressed cellular proliferation, invasion, migration, angiogenesis and stemness in androgen-dependent LNCaP and 22Rv1 cells.Silence of miR-203 or ectopic expression of SNAI2 attenuated the inhibitory effect of PCAT3 and PCAT10 knockdown on cell proliferation and migration in vitro, and xenograft growth in vivo.	Upregulation	LNCaP, 22Rv1	Human	591
CERS6-AS1	ENSG00000227617	lncRNA	35146902	2022	CERS6-AS1 contributes to the malignant phenotypes of colorectal cancer cells by interacting with miR-15b-5p to regulate SPTBN2	colorectal carcinoma (CRC)	CERS6-AS1 and SPTBN2 were highly expressed in colorectal cancer tissues and cells. CERS6-AS1 depletion inhibited cell viability, proliferation, migration, and invasion, the epithelial-mesenchymal transition process and stemness. Sphere-formation assays revealed that the stemness of colorectal cancer cells was inhibited by CERS6-AS1 silencing.	Upregulation	Caco-2, HCT-15	Human	21
SOX21-AS1	ENSG00000227640	lncRNA	33103351	2021	Long non-coding RNA SOX21-AS1 enhances the stemness of breast cancer cells via the Hippo pathway	breast cancer (BRCA)	The expression level of SOX21-AS1 is increased in breast cancer tissues and cell lines, especially in BCSCs. SOX21-AS1 may promote the stemness viability, proliferation, migration and invasion of BCSCs by inhibiting the Hippo pathway.	Upregulation	MCF-7, MDA-MB-231	Human	616
SOX21-AS1	ENSG00000227640	lncRNA	36335356	2022	SOX21-AS1 activated by STAT6 promotes pancreatic cancer progression via up-regulation of SOX21	pancreatic cancer (PaCa)	SOX21-AS1 possessed a high expression level in PC cells. SOX21-AS1 absence suppressed PC cell proliferation, migration, stemness and epithelial-mesenchymal transition (EMT) while elevated cell apoptosis.	Upregulation	CFPAC-1, BxPc3	Human	617
PCAT6	ENSG00000228288	lncRNA	32339330	2020	PCAT6 mediates cellular biological functions in gastrointestinal stromal tumor via upregulation of PRDX5 and activation of Wnt pathway	gastrointestinal stromal tumor (GIST)	Moreover, sphere formation assay measured that PCAT6 knockdown decreased sphere formation efficiency. PCAT6 promoted GIST cell proliferation and stemness but inhibited cell apoptosis via competing endogenous RNA pattern and activation of Wnt pathway.	Upregulation	GIST-882, GIST-T1	Human	590
LINC01013	ENSG00000228495	lncRNA	33847733	2021	Novel role of LINC01013 or miR-6795-5p or FMNL3 axis in the regulation of hepatocellular carcinoma stem cell features	hepatocellular carcinoma (HCC)	HCC tissues showed increased LINC01013 and FMNL3 expression, while it showed a decreased miR-6795-5p expression as compared to the relative controls. Silencing LINC01013, FMNL3, or overexpression of miR-6795-5p could suppress spheroid and colony formation, proliferation, as well as expression of stemness markers in HepG2 and SNU-182 cells. LINC01013 knockdown suppressed growth and stem-like traits of HCC cells in vivo by reducing FMNL3 expression.	Upregulation	HepG2, SNU-182	Human	157
MACC1-AS1	ENSG00000228598	lncRNA	30742067	2019	MSC-regulated lncRNA MACC1-AS1 promotes stemness and chemoresistance through fatty acid oxidation in gastric cancer	gastric cancer (GC)	We found that the expression of MACC1-AS1 was obviously increased both in GC cells and sphere-forming GC cells after co-culture with MSCs. The population of CD44+ GC cells evaluated by flow cytometric analysis was significantly increased and sphere-formation assay showed that sphere-formation capability of GC cells was obviously increased after overexpression of MACC1-AS1. Transforming growth factor beta1 (TGF-beta1) secretion by MSCs activated SMAD2 or 3 through TGF-beta receptors and induced long non-coding RNA (lncRNA) MACC1-AS1 expression in GC cells, which promoted FAO-dependent stemness and chemoresistance through antagonizing miR-145-5p.	Upregulation	AGS, MKN45	Human	194
MACC1-AS1	ENSG00000228598	lncRNA	32339066	2020	Long noncoding RNA MACC1-AS1 promotes the stemness of hepatocellular carcinoma cells by antagonizing miR-145	hepatocellular carcinoma (HCC)	MiR-145 overexpression negatively regulated the expression of stemness master regulators, spheroid formation ability, and ALDH1 activity in clinical samples and cells in the same way that MACC1-AS1 did, and miR-145 expression was negatively correlated with MACC1-AS1 expression in clinical samples. MACC1-AS1 promoted the stemness of HCC cells by antagonizing miR-145 activity. Overexpression of miR-145 also attenuated HCC cell stemness.	Upregulation	SMMC7721, Huh7	Human	195
MACC1-AS1	ENSG00000228598	lncRNA	32058221	2020	The long non-coding RNA MACC1-AS1 promotes nasopharyngeal carcinoma cell stemness via suppressing miR-145-mediated inhibition on SMAD2 or MACC1-AS1 axis	nasopharyngeal carcinoma (NPC)	MACC1-AS1 was highly expressed in NPC tissues and cells relative to the adjacent tissues and nasal mucosa cells, respectively. In vitro and in vivo experiments revealed that MACC1-AS1 knockdown reduced the stemness of NPC cells, which was indicated by the decrease of sphere-forming ability, ALDH1 activity, stemness marker expression and tumor-initiating capacity.	Upregulation	SCC25, HN4	Human	196
MACC1-AS1	ENSG00000228598	lncRNA	32401390	2020	Long noncoding RNA MACC1-AS1 promotes the stemness of nonsmall cell lung cancer cells through promoting UPF1-mediated destabilization of LATS1 or 2	non-small cell lung cancer (NSCLC)	Overexpression of MACC1-AS1 enhanced the stemness of NSCLC cells, which is evident as the increased expression of cancer stem cell transcription factors, ALDH1 activity, and sphere-formation capacity, while knockdown of MACC1-AS1 decreased it. Overexpression of LAST1 or 2 attenuated the promoting effects of MACC1-AS1 overexpression on the stemness of NSCLC cells.	Upregulation	A549, H1299	Human	197
HOTAIR	ENSG00000228630	lncRNA	36273585	2022	Long noncoding RNA HOTAIR regulates the stemness of breast cancer cells via activation of the NF-kappaB signaling pathway	breast cancer (BRCA)	HOTAIR is highly expressed in breast CSCs. Importantly, HOTAIR depletion also dramatically reduced oncosphere formation of MCF7 CSC. HOTAIR overexpression also significantly enhanced oncosphere formation of the CSCs. Additionally, we also found HOTAIR knockdown or NF-kappaB interruption by shp65 or PDTC could abrogate oncosphere formation ability of these CSCs. Our data suggest that HOTAIR-mediated NF-kappaB signaling primes breast CSC self-renewal and tumor propagation. We have identified HOTAIR-based NF-kappaB signaling regulatory circuit that promotes tumorigenic activity in breast CSCs.	Upregulation	MCF7, MDA-MB-453	Human	107
HOTAIR	ENSG00000228630	lncRNA	34470574	2021	HOTAIR regulates colorectal cancer stem cell properties and promotes tumorigenicity by sponging miR-211-5p and modulating FLT-1	colorectal carcinoma (CRC)	HOTAIR was highly expressed and predicted poor prognosis survival in CRC. Sphere formation assay indicated that HOTAIR inhibition led to the reduction of tumor spheres number. Downregulation of HOTAIR repressed tumor malignant behaviors and cancer stemness. HOTAIR or miR-211-5p or FLT-1 axis contributes to CRC cancer stemness.	Upregulation	HCT116, LoVo	Human	108
HOTAIR	ENSG00000228630	lncRNA	34697449	2022	HOTAIR or Sp1 or miR-199a critically regulates cancer stemness and malignant progression of cutaneous squamous cell carcinoma	cutaneous squamous cell carcinoma (CSCC)	We detected higher expression of HOTAIR in CSCC than in normal tissues, in recurrent than in non-recurrent CSCC tissues, in CSCCs and CSCSCs than in HSFs, and particularly, in CSCSCs than in CSCCs. Sphere formation assay revealed that both shHOTAIR_2 and _3 potently thwarted the sphere-forming efficiency of CSCSCs. HOTAIR, by up-regulating Sp1 and targeting miR-199a, promotes stemness and progression of CSCC.	Upregulation	A431, SCC13	Human	109
HOTAIR	ENSG00000228630	lncRNA	29228709	2017	Targeting LncRNA HOTAIR suppresses cancer stemness and metastasis in oral carcinomas stem cells through modulation of EMT	oral squamous cell carcinoma (OSCC)	The expression of HOTAIR was upregulated in tumor tissues, especially in the metastatic samples. Knockdown of HOTAIR in OSCC-CSCs suppressed their secondary sphere-forming ability and reduced ALDH1 activity. Silence of HOTAIR in oral carcinomas stem cells (OCSC) significantly inhibited their cancer stemness, invasiveness and tumourigenicity in xenotransplantation models. Overexpression of HOTAIR in OSCC enhanced their metastatic potential and epithelial-mesenchymal transition (EMT) characteristics.	Upregulation	GNM, Ca9-22	Human	110
HOTAIR	ENSG00000228630	lncRNA	32771526	2020	HOTAIR maintains the stemness of ovarian cancer stem cells via the miR-206 or TBX3 axis	ovarian cancer (OC)	HOTAIR was highly expressed in the OCSCs and its depletion caused a decrease in sphere-formation ability, along with reduced resistance to cisplatin and in vivo tumorigenicity. HOTAIR relieves the inhibition of TBX3 expression mediated by miR-206 in OCSCs.	Upregulation	SKOV3, ES2	Human	111
HOTAIR	ENSG00000228630	lncRNA	33157157	2021	HOTAIR and androgen receptor synergistically increase GLI2 transcription to promote tumor angiogenesis and cancer stemness in renal cell carcinoma	renal cell carcinoma (RCC)	Knockdown of HOTAIR and AR decreased cell sphere formation in SW839 and OSRC-2 cells. HOTAIR-AR enhances the expression of GLI2 downstream CSC transcription factors and promotes cancer stemness in RCC cells. HOTAIR-AR may synergistically promote tumor angiogenesis and cancer stemness in tumor xenografts.	Upregulation	SW839, OSRC-2	Human	112
XIST	ENSG00000229807	lncRNA	30026327	2018	Loss of XIST in Breast Cancer Activates MSN-c-Met and Reprograms Microglia via Exosomal miRNA to Promote Brain Metastasis	breast cancer (BRCA)	XIST was significantly downregulated in brain metastatic tumors. Knockout of XIST in mice mammary glands accelerated primary tumor growth as well as metastases in the brain. Decreased expression of XIST stimulated epithelial-mesenchymal transition and activated c-Met via MSN-mediated protein stabilization, which resulted in the promotion of stemness in the tumor cells.	Downregulation	MCF7, ZR75-1	Human	642
EMX2OS	ENSG00000229847	lncRNA	36722215	2023	EMX2OS targeting IGF2BP1 represses Wilms' tumour stemness,epithelial-mesenchymal transition and metastasis	Wilms' tumour (WT)	EMX2OS was downregulated in WT patients, while IGF2BP1 was upregulated. EMX2OS overexpression or IGF2BP1 knockdown suppressed WT cell sphere formation, migration and invasion.The in vivo tumour growth, stemness and EMT were repressed by EMX2OS through the interaction with IGF2BP1.	Downregulation	17-94, WiT49	Human	77
LINC01315	ENSG00000229891	lncRNA	35156543	2022	LncRNA LINC01315 silencing modulates cancer stem cell properties and epithelial-to-mesenchymal transition in colorectal cancer via miR-484 or DLK1 axis	colorectal carcinoma (CRC)	LINC01315 was high-expressed in CRC and ALDH+ cells. LINC01315 silencing suppressed the migration, invasion, and sphere formation of CRC cells and tumor growth, and downregulated expressions of CSC molecules (ALDH, cluster of difference 44 (CD44), Prominin, and sex determining region Y-box 2 (SOX2), Zinc Finger E-Box Binding Homeobox 1 (ZEB1) and Vimentin but upregulated E-Cadherin expression.	Upregulation	HCT116, SW480	Human	161
LINC01315	ENSG00000229891	lncRNA	35470736	2022	Colorectal cancer stem cell-derived exosomal long intergenic noncoding RNA 01315 (LINC01315) promotes proliferation, migration, and stemness of colorectal cancer cells	colorectal carcinoma (CRC)	LINC01315 was high-expressed in CD133+ or CD44+ colorectal cancer stem cells and exosomes. LINC01315 silencing decreased the viability, proliferation, stemness, and migration of CD133+ or CD44+ cancer cells, while sh-LINC01315 inhibited the promotive effects of CD133+ or CD44+ cancer cell-derived exosomes on the viability, proliferation, stemness, and migration of colorectal cancer cells.	Upregulation	SW480, HCT116	Human	162
FEZF1-AS1	ENSG00000230316	lncRNA	29797562	2018	Long non-coding RNA FEZF1-AS1 promotes breast cancer stemness and tumorigenesis via targeting miR-30a or Nanog axis	breast cancer (BRCA)	In vitro experiments, FEZF1-AS1 was significantly over-expressed in breast cancer cells, especially in sphere subpopulation compared with parental subpopulation. Loss-of-functional indicated that, in BCSC cells (MDA-MB-231 CSC, MCF-7 CSC), FEZF1-AS1 knockdown reduced the CD44+ or CD24- rate, the mammosphere-forming ability, stem factors (Nanog, Oct4, SOX2), and inhibited the proliferation, migration and invasion. In vivo, FEZF1-AS1 knockdown inhibited the breast cancer cells growth.	Upregulation	MCF-7, MDA-MB-231	Human	82
LINC00332	ENSG00000230710	lncRNA	35787995	2022	Inhibitory role of LINC00332 in gastric cancer progression through regulating cell EMT and stemness	gastric cancer (GC)	The expressions of LINC00332 and MMP-13 were significantly downregulated and upregulated in GC tissues. The LINC00332 overexpression markedly repressed proliferation, migration, and invasion. LINC00332 overexpression notably promoted the E-cadherin protein expression.LINC00332 significantly decreased the cisplatin resistance. These results collectively suggested that the LINC00332 overexpression could inhibit the activation of the EMT pathway and decrease the expression of major stemness factors in GC cell line AGS.	Downregulation	AGS	Human	144
FOXD3-AS1	ENSG00000230798	lncRNA	33204001	2020	Long non-coding RNA FOXD3-AS1 silencing exerts tumor suppressive effects in nasopharyngeal carcinoma by downregulating FOXD3 expression via microRNA-185-3p upregulation	nasopharyngeal carcinoma (NPC)	FOXD3-AS1 and FOXD3 exhibited increased expression levels, while miR-185-3p exhibited diminished levels in NPC. FOXD3-AS1 knockdown repressed cell stemness, colony formation, viability, invasion, migration, and in vivo tumor growth, and accelerated cell apoptosisFOXD3 silencing or miR-185-3p overexpression reversed the effects of lncRNA FOXD3-AS1.	Upregulation	C666-1, HK-1	Human	87
LINC01305	ENSG00000231453	lncRNA	33638945	2021	LncRNA LINC01305 promotes cervical cancer progression through KHSRP and exosome-mediated transfer	cervical cancer (CC)	LINC01305 was increased in CC tumor tissues. By applying flow cytometry, we sorted stem-like cell populations from CC tissues through the CD44 surface marker. Then, we found that the expressions of LINC01305, p65, and STAT3 were increased in CD44-positive cells, compared with CD44-negative cells. Meanwhile, in CC tissues with a high level of CD44, we observed a higher level of LINC01305, p65, and STAT3, relative to CC tissues with low expression of CD44. After coculturing with Exo-LINC01305, we found that the protein expressions of beta-catenin, TCF7, and CCND2 were increased in C-33A cells. LINC01305 promotes the progression of CC through KHSRP and that LINC01305 is released through exosomes and is involved in the stemness of CC.	Upregulation	C-33A	Human	160
LINC-PINT	ENSG00000231721	lncRNA	31131448	2019	Long noncoding RNA LINC-PINT regulates laryngeal carcinoma cell stemness and chemoresistance through miR-425-5p or PTCH1 or SHH axis	laryngeal carcinoma (LC)	LINC-PINT expression was downregulated in laryngeal tumors. LINC-PINT was found to be significantly decreased in cell spheres as compared with parental HEp-2 cells. LINC-PINT re-expression in laryngeal tumors may be explored for reversion of cancer cell stemness and also for rescue of drug resistance phenotype.	Downregulation	HEp-2	Human	172
EMBP1	ENSG00000231752	lncRNA	32482375	2020	The long noncoding RNA EMBP1 inhibits the tumor suppressor miR-9-5p and promotes renal cell carcinoma tumorigenesis	renal cell carcinoma (RCC)	Moreover, since the acquisition of EMT is shown to be mechanistically linked with a CSC-like phenotype, we also analyzed the expression of the stemness markers KLF4 and Nanog under miR-9-5p-overexpression conditions. We observed a decrease in KLF4 and Nanog protein levels in both ACHN and Caki-1 cell lines as compared with control, suggesting reduced stemness with miR-9-5p overexpression. MiR-9-5p was significantly down-regulated, and EMBP1 was significantly up-regulated, in RCC cell lines and tumor tissue. Overexpression of miR-9-5p or EMBP1 suppression in RCC cell lines significantly retarded their proliferative, migratory, and invasive behavior, in addition to promoting apoptosis and cell-cycle arrest.	Upregulation	ACHN, Caki-1	Human	76
DLX6-AS1	ENSG00000231764	lncRNA	30442366	2018	LncRNA DLX6-AS1 or miR-129-5p or DLK1 axis aggravates stemness of osteosarcoma through Wnt signaling	osteosarcoma (OS)	DLX6-AS1 enhanced osteosarcoma stemness in vitro and in vivo. DLX6-AS1 competitively interacted with miR-129-5p to DLK1, resulting in activation of Wnt signaling and promotion of stemness in osteosarcoma. DLX6-AS1 functionally interplayed with miR-129-5p to form a reciprocal feedback loop to activate Wnt signaling.	Upregulation	MG63, U2OS	Human	71
LINC00665	ENSG00000232677	lncRNA	33436545	2021	Long non-coding RNA LINC00665 promotes gemcitabine resistance of cholangiocarcinoma (CCA) cells via regulating EMT and stemness properties through miR-424-5p or BCL9L axis	cholangiocarcinoma (CCA)	LINC00665 were found to rank the top 10 upregulated lncRNAs in our study,enforced LINC00665 expression increased gemcitabine resistance of sensitive CCA cells. Silencing LINC00665 suppressed sphere formation, migration, invasion and expression of EMT and stemness markers. LINC00665 knockdown suppressed Wnt or beta-Catenin activation.	Upregulation	HuCCT1, SNU-245	Human	153
HOXB-AS3	ENSG00000233101	lncRNA	35253323	2022	Transcriptional suppression of Dicer by HOXB-AS3 or EZH2 complex dictates sorafenib resistance and cancer stemness	liver cancer (HULC)	Knockdown of Dicer also resulted in recovered expression of OCT4 and SOX2 as well as sphere formation ability in HOXB-AS3-depleted cells. HOXB-AS3 expression was negatively correlated with Dicer expression. HOXB-AS3 expression was positively correlated with the presence of cancer stemness markers, SOX2 and OCT4, in patients.	Upregulation	Huh7	Human	124
LINC-ITGB1	ENSG00000233387	lncRNA	30485693	2019	Knockdown of long non-coding RNA LINC-ITGB1 inhibits cancer stemness and epithelial-mesenchymal transition by reducing the expression of Snail in non-small cell lung cancer	non-small cell lung cancer (NSCLC)	LINC-ITGB1 was greatly upregulated in CSC spheres. These observations suggested that linc-ITGB1 could promote NSCLC cancer stemness by increasing CSC sphere formation and the expression of associated genes. LINC-ITGB1 promoted NSCLC cell EMT and cancer stemness by regulating Snail expression.	Upregulation	A549, L9981	Human	171
HOTAIRM1	ENSG00000233429	lncRNA	31691127	2020	Long Noncoding RNA HOTAIRM1 Maintains Tumorigenicity of Glioblastoma Stem-Like Cells Through Regulation of HOX Gene Expression	glioblastoma (GBM)	HOTAIRM1 is significantly elevated in GSCs. Interestingly, the silencing of HOTAIRM1 also significantly inhibits the neurosphere-forming ability of GSCs. The silencing of HOTAIRM1 significantly impairs the proliferation, apoptosis, self-renewal, tumorigenesis of GSCs.	Upregulation	GSC1, GSC2	Human	113
STXBP5-AS1	ENSG00000233452	lncRNA	33160411	2020	LncRNA STXBP5-AS1 suppresses stem cell-like properties of pancreatic cancer by epigenetically inhibiting neighboring androglobin gene expression	pancreatic cancer (PaCa)	Downregulation of STXBP5-AS1 in PC associated with poor prognosis. The lower abundance of STXBP5-AS1 was especially characterized in sphere derived from these two cells. The lower abundance of STXBP5-AS1 was especially characterized in sphere derived from these two cells. Ectopic STXBP5-AS1 inhibited chemoresistance and metastasis of PC cells. STXBP5-AS1 potently recruited EZH2 and epigenetically regulated neighboring ADGB transcription, which predominantly mediated the inhibitory effects of STXBP5-AS1 on stem cell-like properties of PC cells.	Downregulation	PANC-1, Mia PaCa-2	Human	623
LINC00460	ENSG00000233532	lncRNA	34612153	2021	LncRNA LINC00460 takes a stimulating role on hepatocellular carcinoma stemness property	hepatocellular carcinoma (HCC)	LINC00460 was markedly over-expressed in HCC and silencing LINC00460 impaired cell stemness. We found that LINC00460 overexpression facilitated sphere formation of HCC cells, while LINC00460 knockdown impeded facilitated sphere formation of HCC cells. LINC00460 aggravated cell stemness in HCC via targeting miR-503-5p or miR-654-3p and TCP1.	Upregulation	Huh-7, Hep3b	Human	145
B4GALT1-AS1	ENSG00000233554	lncRNA	30912138	2019	lncRNA B4GALT1-AS1 promotes colon cancer (CC) cell stemness and migration by recruiting YAP to the nucleus and enhancing YAP transcriptional activity	colon cancer (CC)	As the capacity of cell clone formation is associated with cell stemness, we assumed that B4GALT1-AS1 is positively correlated with CC cell stemness. We first defined the B4GALT1-AS1-regulated transcriptome in HCT-116 cells with or without B4GALT1-AS1 knockdown, and we found that the expression of stemness markers of CC (ALDH1, Nanog, CD110, LGR5, CD44, CD133, and EpCAM) was remarkably reduced in cells with B4GALT1-AS1 knockdown. Furthermore, the cell spheroid formation assay demonstrated that B4GALT1-AS1 knockdown attenuated spheroid formation capacity, evidenced by the decrease of spheroid size and number.	Upregulation	HCT-116, HT-29	Human	11
B4GALT1-AS1	ENSG00000233554	lncRNA	30182452	2018	LncRNA B4GALT1-AS1 recruits HuR to promote osteosarcoma cells stemness and migration via enhancing YAP transcriptional activity	osteosarcoma (OS)	We further investigated whether B4GALT1-AS1 promoted OS cells stemness. We found that B4GALT1-AS1 knockdown inhibited the expression of tumour stemness markers (Nanog and ALDH1). Meanwhile, the potential of cell spheroid formation was remarkably attenuated by B4GALT1-AS1 knockdown in OS cells, characterized as the decrease in spheres size and number. In addition, the activity of ALDH1 was also downregulated in OS cells with B4GALT1-AS1 knockdown via ALDH activity assay kit analysis. Thus, our results suggest that B4GALT1-AS1 could facilitate OS cells progression.	Upregulation	MG63, U2OS	Human	12
LINC01426	ENSG00000234380	lncRNA	33568633	2021	Upregulation of LINC01426 promotes the progression and stemness in lung adenocarcinoma by enhancing the level of SHH protein to activate the hedgehog pathway	lung adenocarcinoma (LUAD)	The expression of LINC01426 was upregulated in LUAD tissue. Silencing of LINC01426 obviously suppressed the proliferation, migration, epithelial-mesenchymal transition (EMT), and stemness of LUAD cells. Sphere formation assay further certified that LINC01426 knockdown suppressed the sphere formation capacity of PC-9 and Calu3 cells.	Upregulation	PC-9, Calu3	Human	164
GAS5	ENSG00000234741	lncRNA	32269616	2020	Long non-coding RNA GAS5 is critical for maintaining stemness and induces chemoresistance in cancer stem-like cells derived from HCT116	colorectal carcinoma (CRC)	However, the serial replating assay suggested that knockdown of GAS5 abolished sphere formation ability. GAS5 knockdown by specific siRNA significantly decreased CSC self-renewal capacity, proliferation and migration. GAS5 knockdown sensitized CSCs to the chemotherapeutic agents 5-fluorouracil and doxorubicin by inducing apoptosis detected by Annexin V-FITC or PI double staining.	Upregulation	HCT116	Human	89
SNHG20	ENSG00000234912	lncRNA	30943748	2019	LncRNA SNHG20 promotes tumorigenesis and cancer stemness in glioblastoma via activating PI3K or Akt or mTOR signaling pathway	glioblastoma (GBM)	SNHG20 was significantly upregulated in glioblastoma tissues and cell lines. SNHG20 knockdown obviously suppressed cell proliferation, increased cell apoptosis and impaired stem properties. SNHG20 regulated PI3K or Akt or mTOR signaling pathway to promote tumorigenesis and stemness of glioblastoma. The results of sphere forming assay indicated that knockdown of SNHG20 obviously impaired the ability of sphere formation of LN215 and U251 cells.	Upregulation	U251, LN215	Human	610
SNHG20	ENSG00000234912	lncRNA	30394668	2019	Long non-coding RNA SNHG20 promotes the tumorigenesis of oral squamous cell carcinoma via targeting miR-197 or LIN28 axis	oral squamous cell carcinoma (OSCC)	LncRNA SNHG20 was up-regulated in OSCC tissue compared with adjacent non-tumour tissue. Meanwhile, SNHG20 was overexpressed in cancer stem-like cells. SNHG20 knockdown inhibited proliferative ability, mammosphere-forming ability, ALDH1 expression, stem factors and tumour growth.	Upregulation	SCC9, SCC15, SCC25, Ca9-22, HSU3, TSCCA, Fadu	Human	611
LINC00941	ENSG00000235884	lncRNA	36717549	2023	Reciprocal regulation of LINC00941 and SOX2 promotes progression of esophageal squamous cell carcinoma	esophageal squamous cell carcinoma (ESCC)	LINC00941 was significantly upregulated in ESCC, and upregulated LINC00941 was correlated with dismal patient outcomes. Furthermore, the sphere-formation abilities of the siLINC00941 transfected KYSE-170 cells were significantly inhibited, while the LINC00941 overexpressed TE-1 cells were evidently stimulated. LINC00941 functioned as an oncogene by promoting cells proliferation, stemness, migration, and invasion in ESCC. LINC00941 exacerbates ESCC progression through forming a LINC00941-ILF2 or YBX1-SOX2 positive feedback loop.	Upregulation	KYSE-170, TE-1	Human	155
PITPNA-AS1	ENSG00000236618	lncRNA	35588441	2022	LncRNA PITPNA-AS1 or miR-223-3p or PTN axis regulates malignant progression and stemness in lung squamous cell carcinoma	lung squamous cell carcinoma (LUSC)	The lncRNA PITPNA-AS1 had increased expression in LUSC and was linked to a poor prognosis. PITPNA-AS1 increased LUSC cell proliferation, migration, invasion, and stemness. PITPNA-AS1 upregulated PTN through sponging miR-223-3p to enhance the onset and progression of LUSC.	Upregulation	SK-MES-1, NCI-H520, NCI-H226, NCI-H2170, BEAS-2B	Human	593
BC200	ENSG00000236824	lncRNA	32784466	2020	Targeting BC200 or miR218-5p Signaling Axis for Overcoming Temozolomide Resistance and Suppressing Glioma Stemness	glioblastoma (GBM)	To definitively understand the role of BC200 in GB, we knocked down BC200 RNA and examined its effect on cell migration, motility, and invasion. Moreover, the self-renewal capacity was suppressed because of BC200 RNA inhibition, indicated through significant reduction in colony-forming ability, but no effect on cell proliferation and neurosphere generation in comparison with mock-transfected control groups. Furthermore, the effect of BC200 RNA inhibition was evaluated on marker expression associated with the self-renewal and pluripotency of GB cells, such as Oct4, SOX2, and KLF4 [24], which were observed to be downregulated in BC200-suppressed cells in comparison with control mock-transfected cells.	Upregulation	T98, GBM8901	Human	13
BC200	ENSG00000236824	lncRNA	30400024	2018	Thyroid hormone negatively regulates tumorigenesis through suppression of BC200	hepatocellular carcinoma (HCC)	As specified earlier, TICs have the capacity to self-renew and regenerate new tumors. To determine the association between TIC behavior and BC200, flow cytometry of the CD133+ TIC population in HCC cell lines was performed. HepG2 and Huh7 cell lines were further sorted into CD133- and CD133+ populations and confirmed via western blot. BC200 was upregulated in CD133+ HepG2 cells. To determine whether BC200 functions in liver TIC self-renewal, the sphere formation assay was performed. Knockdown of BC200 dramatically reduced the tumor sphere formation frequencies of CD133+ subsets of HepG2 and Huh7 cells, compared with sh-luc cells. In view of these results, we propose that BC200 is required for maintaining stemness ability in HCC.	Upregulation	HepG2, Huh7	Human	14
LINC00106	ENSG00000236871	lncRNA	34858996	2021	M6A-Mediated Upregulation of LINC00106 Promotes Stemness and Metastasis Properties of Hepatocellular Carcinoma via Sponging Let7f	hepatocellular carcinoma (HCC)	LINC00106 was prominently upregulated in tissues and cell lines of HCC. The sphere (primary and secondary) formation capabilities were weakened by abnormal LINC00106 suppression in MHCC-97H and SNU-449 cells compared with that in the control cells. By contrast, in Huh7 cells, the sphere (primary and secondary) formation capabilities were enhanced due to LINC00106 overexpression. m6A methylation triggers the upregulation of LINC00106, which promotes the stemness and metastasis properties in HCC cells by sponging let7f, thereby resulting in periostin activation.	Upregulation	MHCC-97H, SNU-449, Huh7	Human	141
MIR600HG	ENSG00000236901	lncRNA	32270866	2020	MIR600HG suppresses metastasis and enhances oxaliplatin chemosensitivity by targeting ALDH1A3 in colorectal cancer	colorectal carcinoma (CRC)	We detected down-regulated expression of lncRNA MIR600HG in CRC specimens and cell lines compared with normal controls. Inhibition of MIR600HG stimulated CRC stemness. MIR600HG functions as a tumour suppressor and that the overexpression of MIR600HG inhibits tumour invasion and enhances chemosensitivity.	Downregulation	Caco2	Human	537
ZEB1-AS1	ENSG00000237036	lncRNA	31978895	2020	AR-induced ZEB1-AS1 represents poor prognosis in cholangiocarcinoma (CCA) and facilitates tumor stemness, proliferation and invasion through mediating miR-133b or HOXB8	cholangiocarcinoma (CCA)	ZEB1-AS1 expression was increased in CCA tissues and cells, respectively.Knocking down ZEB1-AS1 attenuated tumor cell stemness, restrained cellular viability in vitro and in vivo, and inhibited CCA cell migration and invasion by reversing epithelial-mesenchymal transition.	Upregulation	QBC939, CCLP-1	Human	644
HCP5	ENSG00000237105	lncRNA	34190001	2021	LncRNA HCP5 promotes malignant cell behaviors in esophageal squamous cell carcinoma via the PI3K or AKT or mTOR signaling	esophageal squamous cell carcinoma (ESCC)	HCP5 expression was at a higher level in ESCC tissues and cells compared to that in control tissues and cells. Results of sphere formation assay showed reduction in sphere number in sh-HCP5_1-transfected KYSE30 and EC109 cells, indicating that ESCC cell stemness characteristics were suppressed by HCP5 deficiency. HCP5 promotes ESCC cellular development by modulating the miR-139-5p or PDE4A pathway and stimulating the PI3K or AKT or mTOR signaling pathway.	Upregulation	KYSE30, EC109	Human	103
HCP5	ENSG00000237105	lncRNA	32300102	2020	MSC-induced lncRNA HCP5 drove fatty acid oxidation through miR-3619-5p or AMPK or PGC1 alpha or CEBPB axis to promote stemness and chemo-resistance of gastric cancer	gastric cancer (GC)	It turned out that in both GC cells and the tumor spheres generated by GC cells, the expression of HCP5, rather than AFAP1-AS1, was upregulated under the co-culture with MSCs versus control. Besides, upregulating HCP5 in GC cells induced sphere formation. MSC-induced lncRNA HCP5 drove FAO through miR-3619-5p or AMPK or PGC1alpha or CEBPB axis to promote stemness and chemo-resistance of GC.	Upregulation	MNK45, AGS	Human	104
HAND2-AS1	ENSG00000237125	lncRNA	30509963	2019	LncRNA HAND2-AS1 inhibits non-small cell lung cancer migration, invasion and maintains cell stemness through the interactions with TGF-beta1	non-small cell lung cancer (NSCLC)	Levels of HAND2-AS1 were lower in tumor tissues than that in adjacent healthy tissues. HAND2-AS1 may regulate the migration, invasion and stemness of NSCLC cells through interactions with TGF-beta1. LncRNA HAND2-AS1 and TGF-beta1 play opposite roles in the migration, invasion and stemness of cells of NSCLC cell lines H1581 and H1993.	Downregulation	H1581, H1993	Human	102
FOXD2-AS1	ENSG00000237424	lncRNA	30520141	2019	Long noncoding RNA FOXD2-AS1 promotes glioma malignancy and tumorigenesis via targeting miR-185-5p or CCND2 axis	glioma	FOXD2-AS1 was upregulated in glioma tissue, cells, and sphere subpopulation. Downregulation of FOXD2-AS1 decreased cell proliferation, migration, invasion, stemness, and epithelial-mesenchymal transition in glioma cells and inhibited tumor growth in transplanted tumor.	Upregulation	U87, U251	Human	84
FOXD2-AS1	ENSG00000237424	lncRNA	35419917	2022	Overexpression of FOXD2-AS1 enhances proliferation and impairs differentiation of glioma stem cells by activating the NOTCH pathway via TAF-1	glioma	FOXD2-AS1, TAF-1 and NOTCH1 were found to be elevated in glioma tissues and GSCs, and silencing lncRNA FOXD2-AS1 inhibited stemness and proliferation, while promoting apoptosis and differentiation of GSCs. FOXD2-AS1 overexpression also led to increased NOTCH1 by recruiting TAF-1 to the NOTCH1 promoter region, thereby promoting stemness and proliferation, while impairing cell apoptosis and differentiation. Sphere formation assays revealed a drastically enhanced sphere forming ability of U251 GSCs in the presence of oe-lncRNA FOXD2-AS1, which could be reversed when treated with oe-lncRNA FOXD2-AS1 + sh-TAF-1. The number of main spheres in every 1000 GSCs and the secondary spheres of every 100 GSCs was increased in response to oe-lncRNA FOXD2-AS1, which was restored following treatment of oe-lncRNA FOXD2-AS1 + sh-TAF-1.	Upregulation	U251	Human	85
FOXD2-AS1	ENSG00000237424	lncRNA	31959918	2020	Long noncoding RNA FOXD2-AS1 enhances chemotherapeutic resistance of laryngeal squamous cell carcinoma via STAT3 activation	laryngeal squamous cell carcinoma (LSCC)	LSCC chemotherapy-resistant patients showed increased FOXD2-AS1 expression compared with that in chemotherapy-sensitive patients, which predicted poor prognosis.U.pregulated FOXD2-AS1 maintained cancer stemness, reducing the response to chemotherapy. Intriguingly, we found that upregulation of FOXD2-AS1 dramatically increased the size and number of spheres among Hep-2 cells, while knockdown of FOXD2-AS1 suppressed sphere formation.	Upregulation	Hep-2, Tu-212	Human	86
KCNMB2-AS1	ENSG00000237978	lncRNA	34516362	2021	Long noncoding RNA KCNMB2-AS1 promotes the development of esophageal cancer by modulating the miR-3194-3p or PYGL axis	esophageal cancer (ESCA)	KCNMB2-AS1 was significantly upregulated in ESCA. As shown by sphere formation assay, silencing of KCNMB2-AS1 reduced the number of spheroids, indicating that the sphere-forming ability of ESCA cells was attenuated. KCNMB2-AS1 downregulation suppressed the growth, invasion, migration and stemness of ESCA cells. LncRNA KCNMB2-AS1 promotes ESCA development through targeting the miR-3194-3p or PYGL axis.	Upregulation	Eca109, TE-1	Human	130
NCK1-AS1	ENSG00000239213	lncRNA	33974352	2021	LncRNA NCK1-AS1 exerts oncogenic property in gastric cancer by targeting the miR-22-3p or BCL9 axis to activate the Wnt or beta-catenin signaling	gastric cancer (GC)	NCK1-AS1 exhibited high expression in gastric cancer tissues and cells. In vitro assays including MTT, colony formation, Transwell, wound healing and sphere formation assays indicated that NCK1-AS1 depletion inhibited cell proliferation, migration, invasion and stemness maintenance. NCK1-AS1 functions as an oncogene and promotes gastric cancer progression via the miR-22-3p or BCL9-Wnt or beta-catenin signaling pathway.	Upregulation	HGC-27, NCI-N87	Human	580
CDKN2B-AS1	ENSG00000240498	lncRNA	36582605	2022	Cancer stem cell-like cells-derived exosomal lncRNA CDKN2B-AS1 promotes biological characteristics in thyroid cancer via miR-122-5p or P4HA1 axis	thyroid cancer	The CDKN2B-AS1 content was the most abundant in TPC-1 and SW579 cells among other cells, so these two cells were selected for further experiments. The transfection of CDKN2B-AS1 silencing plasmid reduced the level of CDKN2B-AS1 in TPC-1 and SW579 cells. sh-CDKN2B-AS1 hindered tumor sphere formation.	Upregulation	TPC-1, SW579	Human	20
HOXA11-AS	ENSG00000240990	lncRNA	27792998	2016	The long noncoding RNA HOXA11 antisense induces tumor progression and stemness maintenance in cervical cancer	cervical cancer (CC)	HOXA11-AS expression was significantly greater in tissues from patients with cervical cancer than in control patients. After 7 days of incubation in anchorage-independent conditions, the control cells presented an elevated number of large colonies, while the HOXA11-AS-silenced cells formed only a few colonies of small size. Counting of colonies revealed a reduction in sphere formation. HOXA11-AS knockdown inhibited these biologic aggressive features. HOXA11-AS knockdown decreased cancer stemness and triggered the EMT program.	Upregulation	HeLa, CaSki	Human	118
HOXA11-AS	ENSG00000240990	lncRNA	31757938	2019	Silencing of long noncoding RNA HOXA11-AS inhibits the Wnt signaling pathway via the upregulation of HOXA11 and thereby inhibits the proliferation, invasion, and self-renewal of hepatocellular carcinoma stem cells	hepatocellular carcinoma (HCC)	HCC stem cells showed high expression of HOXA11-AS and low expression of HOXA11. HOXA11-AS silencing exerts an antitumor effect, suppressing HCC development via Wnt signaling pathway inactivation by decreasing the methylation level of the HOXA11 promoter. HCC stem cells showed high expression of HOXA11-AS and low expression of HOXA11. The number of tumorspheres, cell colonies, invaded cells, and proliferative cells were decreased in the sh-HOCA11-AS group compared with the sh-NC group (all p<0.05).	Upregulation	Hep3B, Huh7	Human	119
HOXA11-AS	ENSG00000240990	lncRNA	36142607	2022	An Axis between the Long Non-Coding RNA HOXA11-AS and NQOs Enhances Metastatic Ability in Oral Squamous Cell Carcinoma	oral squamous cell carcinoma (OSCC)	HOXA11-AS knockdown reduced cell proliferation and invasive capacity to a more pronounced extent in HSC3 cells. Apoptosis was increased in both cell types, while sphere-forming ability was decreased by knockdown of HOXA11-AS, and the changes in both assays occurred to a greater degree in HSC3 compared to HSC4 cells.	Upregulation	HSC3, HSC4	Human	120
ADAMTS9-AS1	ENSG00000241158	lncRNA	36449154	2022	ADAMTS9-AS1 Long Non-coding RNA Sponges miR-128 and miR-150 to Regulate Ras or MAPK Signaling Pathway in Glioma	glioma	Stemness characteristics of the cell are elevated during the EMT process and therefore, the expression level of stemness marker genes was also measured following the ADAMTS9-AS1 overexpression. RT-qPCR results indicated that Sox2 and NANOG marker genes expression level has been increased in both U87 and 1321N1 cell lines. The PAX6 expression level was also signifcantly increased in the U87 cells. Overall, the results of this section revealed the positive efect of ADAMTS9-AS1 on the migration and stemness of U87 and 1321N1 cell lines.	Upregulation	U87, 1321N1	Human	1
HNF1A-AS1	ENSG00000241388	lncRNA	35188404	2022	sh-HNF1A-AS1 reduces the epithelial-mesenchymal transition and stemness of esophageal cancer cells	esophageal squamous cell carcinoma (ESCC)	HNF1A-AS1 was overexpressed in ESCC tumor tissues and cells. The diameter of a sphere in the sh-HNF1A-AS1 group was much smaller than that in the control group. Knockdown of HNF1A-AS1 could inhibit EMT and stemness by regulating the miR-298 or TCF4 axis.	Upregulation	EC109, KYSE-70	Human	106
PTPRG-AS1	ENSG00000241472	lncRNA	34676588	2022	LncRNA PTPRG-AS1 facilitates glycolysis and stemness properties of esophageal squamous cell carcinoma cells through miR-599 or PDK1 axis	esophageal squamous cell carcinoma (ESCC)	PTPRG-AS1 sponged miR-599 to up-regulate PDK1 expression, thereby promoting the proliferation and migration as well as glycolysis and stemness properties of ESCC cells. It was observed through sphere formation assay that the cell sphere formation efficiency and sphere diameter of TE-8 and KYSE-150 cells were both decreased by PTPRG-AS1 depletion.	Upregulation	TE-8, KYSE-150	Human	594
SOX2OT	ENSG00000242808	lncRNA	32019566	2020	Long non-coding RNA SOX2OT promotes the stemness phenotype of bladder cancer cells by modulating SOX2	bladder cancer (BLCA)	SOX2OT was highly expressed in bladder cancer. Knockdown of SOX2OT inhibited the stemness phenotype of BCSCs, and inhibition of SOX2OT delayed xenograft tumour growth and decreased metastases in vivo. Overexpressing SOX2 significantly reversed the spheroid-formation ability inhibition induced by silencing SOX2OT.	Upregulation	SW780, 5637	Human	618
SOX2OT	ENSG00000242808	lncRNA	36548179	2022	SOX2OT lncRNA Inhibition Suppresses the Stemness Characteristics of Esophageal Tumorspheres	esophageal squamous cell carcinoma (ESCC)	ESCC tumorspheres overexpress SOX2OT gene along with other stemness genes (SOX2, OCT4A, and Nanog) compared to their original cancer cells. RNAi experiments indicated that SOX2OT knockdown can suppress the stemness-related gene expression, sphere formation ability (both size and number), and docetaxel resistance as three of the main cancer stem cell characteristics of tumorspheres.	Upregulation	YM1, KYSE30	Human	619
SOX2OT	ENSG00000242808	lncRNA	29475441	2018	SOX2OT variant 7 contributes to the synergistic interaction between EGCG and Doxorubicin to kill osteosarcoma via autophagy and stemness inhibition	osteosarcoma (OS)	EGCG could reduce the Doxorubicin-induced pro-survival autophagy through decreasing SOX2OT variant 7 to improve the growth inhibition of Doxorubicin. EGCG could partially inactivate Notch3 or DLL3 signaling cascade targeting SOX2OT variant 7 to reduce the stemness then abated drug-resistance of osteosarcoma cells.	Upregulation	U2OS, SaoS2	Human	620
MNX1-AS1	ENSG00000243479	lncRNA	35819746	2023	Activation of MYO1G by lncRNA MNX1-AS1 Drives the Progression in Lung Cancer	lung adenocarcinoma (LUAD)	MNX1-AS1was found to be highly expressed in lung cancer tissues and cells. Deletion of MNX1-AS1 inhibited proliferation, migration, invasion and sphere-forming abilities of CSC. MNX1-AS1 suppression significantly repressed the growth of xenografts in vivo.	Upregulation	A549, H2170	Human	579
DUBR	ENSG00000243701	lncRNA	34958891	2022	SP1-induced lncRNA DUBR promotes stemness and oxaliplatin resistance of hepatocellular carcinoma via E2F1-CIP2A feedback	hepatocellular carcinoma (HCC)	DPPA2 upstream binding RNA (DUBR) and its high expression in HCC tissues and liver CSCs. DUBR facilitated the stemness and oxaliplatin resistance of HCC in vitro and in vivo. We identified SP1 or DUBR or E2F1-CIP2A as a critical axis to activate the Notch1 signaling pathway and promote stemness and chemoresistance of HCC.	Upregulation	MHCC-97H, SNU-368	Human	73
HOTTIP	ENSG00000243766	lncRNA	32307830	2020	LncRNA HOTTIP facilitates the stemness of breast cancer via regulation of miR-148a-3p or WNT1 pathway	breast cancer (BRCA)	HOTTIP was markedly up-regulated in BCSCs and had a positive correlation with breast cancer progression. Flow cytometric analysis revealed that the knockdown of HOTTIP dramatically decreased the population of CD44+ or CD24 cells in the sphere cells. We found that the inhibitory effects of depletion of HOTTIP on the self-renewal capacity of MCF7 and T47D sphere cells were reversed by the miR-148a-3p inhibitor in sphere formation assays. HOTTIP directly binds to miR-148a-3p and inhibits the mediation of WNT1, which leads to inactivation of the Wnt or beta-catenin signalling pathway. Knockdown of HOTTIP inhibited the CSC-like properties of BCSCs.	Upregulation	MCF7, T47D	Human	114
HOTTIP	ENSG00000243766	lncRNA	28947139	2017	LncRNA HOTTIP modulates cancer stem cell properties in human pancreatic cancer by regulating HOXA9	pancreatic cancer (PaCa)	HOTTIP was highly expressed in PCSCs. In addition, in vitro assays showed that HOTTIP alterations affected stemness, including sphericity, tumorigenesis, and stem factors (LIN28, NANOG, OCT4, and SOX2) and markers (ALDH1, CD44, and CD133).	Upregulation	PANC-1, SW1990	Human	115
GATA2-AS1	ENSG00000244300	lncRNA	35752837	2022	A feedback loop between GATA2-AS1 and GATA2 promotes colorectal cancer cell proliferation, invasion, epithelial-mesenchymal transition and stemness via recruiting DDX3X	colorectal carcinoma (CRC)	GATA2-AS1 and GATA2 were highly expressed in CRC cells. Knockdown of GATA2-AS1 and GATA2 impeded CRC cell proliferation, invasion, EMT and cancer stemness, and induced cell apoptosis. In addition, the data from western blot analysis and sphere formation assay disclosed that the protein levels of stem cell markers (Nanog and OCT4) and the number and size of spheres were overtly reduced after GATA2-AS1 or GATA2 knockdown. Our study confirmed that a feedback loop between GATA2-AS1 and GATA2 promotes CRC progression.	Upregulation	SW480, HCT116	Human	91
DUXAP10	ENSG00000244306	lncRNA	33340249	2021	Long noncoding RNA DUXAP10 promotes the stemness of glioma cells by recruiting HuR to enhance Sox12 mRNA stability	glioma	DUXAP10 is overexpressed in glioma tissues and cells. DUXAP10 knockdown significantly reduces the stemness of glioma cells, which is characterized as the decrease of stemness marker expression, tumor sphere-forming ability, and ALDH activity. HuR or Sox12 axis is responsible for DUXAP10-mediated effects on glioma cell stemness.	Upregulation	U251, T98G	Human	74
NEAT1	ENSG00000245532	lncRNA	33168814	2020	LncRNA NEAT1 remodels chromatin to promote the 5-Fu resistance by maintaining colorectal cancer stemness	colorectal carcinoma (CRC)	NEAT1 promoted 5-Fu resistance and cancer stemness by remodeling chromatin. Knocking down NEAT1 significantly reduced its spheroid diameter.	Upregulation	HCT116, SW480	Human	581
NEAT1	ENSG00000245532	lncRNA	28615056	2017	Oct4 transcriptionally regulates the expression of long non-coding RNAs NEAT1 and MALAT1 to promote lung cancer progression	lung cancer (LC)	Lung cancer cells overexpressing NEAT1 or MALAT1 and the Oct4-silenced cells reconstituted with NEAT1 or MALAT1 promoted cell proliferation, migration and invasion. In addition, knockdown of NEAT1 or MALAT1 abolished Oct5-mediated lung cancer cell growth and motility.	Upregulation	A549, CL1-0	Human	582
NEAT1	ENSG00000245532	lncRNA	30894512	2019	Long non-coding RNA NEAT1 confers oncogenic role in triple-negative breast cancer through modulating chemoresistance and cancer stemness	triple negative breast cancer (TNBC)	The expression of NEAT1 was higher in TNBC tissues than other subgroups. NEAT1 conferred oncogenic role by regulating apoptosis and cell cycle progression in TNBC cells. ShNEAT1 reduced stem cell populations such as CD44+ or CD24-, ALDH+, and SOX2+, implicating that NEAT1 was closely related to cancer stemness in TNBC.	Upregulation	MDA-MB-231	Human	583
LINC02273	ENSG00000245954	lncRNA	35132378	2022	LINC02273 Promotes Hepatocellular Carcinoma Progression via Retaining beta-Catenin in the Nucleus to Augment Wnt Signaling	hepatocellular carcinoma (HCC)	LINC02273 played a critical role in HCC progression via stabilizing beta-catenin. We observed that knockdown of LINC02273 significantly inhibits proliferation, colony, and sphere formation abilities in both Hep3B and MHCC97H. Knockdown of LINC02237 remarkably inhibited the proliferation, stemness, migration, and invasion abilities, whereas it increased the apoptosis of HCC cells.	Upregulation	Hep3B, MHCC97H	Human	168
OIP5-AS1	ENSG00000247556	lncRNA	35255389	2022	LncRNA OIP5-AS1 aggravates the stemness of hepatoblastoma through recruiting PTBP1 to increase the stability of beta-catenin	hepatoblastoma	OIP5-AS1 was significantly up-regulated in hepatoblastoma cells. OIP5-AS1 silencing notably attenuated the stemness and invasion of hepatoblastoma cells. OIP5-AS1 silencing inhibits the growth and stemness of hepatoblastoma through binding with PTBP1 to inhibit beta-catenin signaling pathway.	Upregulation	HepG2, Huh6	Human	586
OIP5-AS1	ENSG00000247556	lncRNA	35044041	2022	Long noncoding RNA OIP5-AS1 promotes the stemness of lung cancer cells through enhancing Oct4 mRNA stability	lung cancer (LC)	lncRNA OIP5-AS1 was found to be highly expressed in lung cancer cell spheres. Following experiments showed that OIP-AS1 knockdown reduced the CSC-like traits of lung cancer spheres, while overexpression of OIP-AS1 conferred the CSC-like traits in lung cancer cells by performing sphere-formation analysis, detecting stemness marker expression, and ALDH activity by directly interacting with Oct4 mRNA.	Upregulation	A549	Human	587
NR2F2-AS1	ENSG00000247809	lncRNA	32109138	2020	LncRNA NR2F2-AS1 Upregulates Rac1 to Increase Cancer Stemness in Clear Cell Renal Cell Carcinoma	clear cell renal cell carcinoma (ccRCC)	NR2F2-AS1 was upregulated in ccRCC, and high NR2F2-AS1 expression levels in ccRCC tissues were associated with poor survival. NR2F2-AS1 may upregulate Rac1 to increase cancer stemness in ccRCC. NR2F2-AS1 and Rac1 positively regulated 786-O and Caki-1 cell stemness.	Upregulation	786-O, Caki-1	Human	585
LUCAT1	ENSG00000248323	lncRNA	31300015	2019	Long non-coding RNA LUCAT1 or miR-5582-3p or TCF7L2 axis regulates breast cancer stemness via Wnt or beta-catenin pathway	breast cancer (BRCA)	LUCAT1 was more expressed in BCSCs than in breast cancer cells (BCCs) by lncRNA microarray chips. LUCAT1 up-regulation promoted proliferation of BCCs, while LUCAT1 down-regulation inhibited self-renewal of BCSCs. We evaluated CSCs self-renewal ability by sphere-formation assay and found LUCAT1 silencing reduced mammosphere diameter and quantity. LUCAT1 increased stem-like properties of BCCs and stemness of BCSCs by competitively binding miR-5582-3p with TCF7L2 and enhancing the Wnt or beta-catenin pathway.	Upregulation	MCF-7, T47D	Human	192
LUCAT1	ENSG00000248323	lncRNA	35711895	2022	lncRNA LUCAT1 or ELAVL1 or LIN28B or SOX2 Positive Feedback Loop Promotes Cell Stemness in Triple-Negative Breast Cancer	triple negative breast cancer (TNBC)	LUCAT1 is significantly overexpressed in TNBC cells. Meanwhile, spheroid-formation and flow cytometry assays disclosed that cell stemness was inhibited due to LUCAT1 silencing. LUCAT1 interference impedes cell stemness in TNBC cells. The lncRNA LUCAT1 or ELAVL1 or LIN28B or SOX2 positive feedback loop promotes cell stemness in TNBC.	Upregulation	BT-549, MDA-MB-453	Human	193
lncTCF7	ENSG00000249073	lncRNA	29234033	2017	lncTCF7 is a negative prognostic factor, and knockdown of lncTCF7 inhibits migration, proliferation and tumorigenicity in glioma	glioma	lncTCF7 expression was increased in glioma tissues compared with that in normal brain tissues (P<0.001). Loss of function assays revealed that knockdown of lncTCF7 significantly inhibited glioma cell migration, proliferation and tumorigenicity in vitro and in vivo.	Upregulation	U87, U251	Human	187
C5orf66-AS1	ENSG00000249082	lncRNA	34431063	2021	Mesenchymal stem cell-derived exosomes block malignant behaviors of hepatocellular carcinoma stem cells through a lncRNA C5orf66-AS1 or microRNA-127-3p or DUSP1 or ERK axis	hepatocellular carcinoma (HCC)	Exo treatment reduces angiogenesis and self-renewal ability of the CSCs. The C5orf66-AS1 expression in HuH7-CSC was signifcantly elevated after Exo treatment. Exo treatment enhanced the C5orf66-AS1 expression in CSCs by exogenous addition rather than endogenous induction.	Downregulation	HuH7, Hep3B	Human	15
CASC11	ENSG00000249375	lncRNA	30965130	2019	LncRNA CASC11 promotes TGF-beta1, increases cancer cell stemness and predicts postoperative survival in small cell lung cancer	small cell lung cancer (SCLC)	Comparing to control (C) and negative control (NC) group, overexpression of lncRNA CASC11 and TGF-beta1 (10 ng or ml) treatment led to increased percentage of CDD133+ cells of cells of SCLC SHP-77 and DMS 79 cell lines, while treatment with TGF-beta inhibitor SB431542 (SB, Sigma-Aldrich) at a dose of 10 nM attenuated the effects of CASC11 overexpression. In addition, lncRNA CASC11 silencing led to decreased percentage of CDD133+ cells of both SHP77 and DMS79 cell lines.	Upregulation	SHP-77, DMS-79	Human	16
LINC00942	ENSG00000249628	lncRNA	35073459	2022	LncRNA LINC00942 promotes chemoresistance in gastric cancer by suppressing MSI2 degradation to enhance c-Myc mRNA stability	gastric cancer (GC)	LNC942 was found to be up-regulated in chemoresistant GC cells, and its high expression was positively correlated with the poor prognosis of patients with GC. Interestingly, the number and size of spheres were found to be decreased in SGC7901 cells compared with those in SGC-R cells. Consistently, LNC942 depletion dramatically reduced the oncosphere formation of SCG-R cells. Functional studies indicated that LNC942 confers chemoresistance to GC cells by impairing apoptosis and inducing stemness.	Upregulation	SGC7901	Human	156
PVT1	ENSG00000249859	lncRNA	34336125	2021	Exosomal lncRNA PVT1 or VEGFA Axis Promotes colon cancer (CC) Metastasis and Stemness by Downregulation of Tumor Suppressor miR-152-3p	colon cancer (CC)	In vitro silencing of PVT1 reduced colon tumorigenic properties including migratory, invasive, colony forming, and tumorsphere generation abilities. Exosomal PVT1 promotes colon cancer (CC) metastasis through its association with EGFR and VEGFA expression.	Upregulation	HCT116, LoVo	Human	595
PVT1	ENSG00000249859	lncRNA	34230224	2021	Long Noncoding RNA PVT1 Promotes Stemness and Temozolomide Resistance through miR-365 or ELF4 or SOX2 Axis in Glioma	glioma	Elevated PVT1 expression was observed in glioma tissues and cells. Knockdown of PVT1 and overexpression of miR-365 inhibited proliferation, migration, invasion and promoted stemness and Temozolomide (TMZ) resistance of glioma cells. PVT1 promoted glioma stemness through miR-365 or ELF4 or SOX2 axis.	Upregulation	U87, U251	Human	596
PVT1	ENSG00000249859	lncRNA	30141114	2019	Non-Coding RNA Pvt1 Promotes Cancer Stem Cell-Like Traits in Nasopharyngeal Cancer via Inhibiting miR-1207	nasopharyngeal carcinoma (NPC)	PVT1 was significantly up-regulated in both NPC tissues and cell lines and associated with poor prognosis. PVT1 knockdown reduced NPC cells viability, clonogenicity, the cell surface CD44+ or CD24- stem phenotype, and the expressions of the stem cell markers in NPC cells, including Oct4, c-Myc, SOX2, and ALDH. The tumor-sphere formation assay showed that PVT1 siRNAs transfection reduced the ability of NPC cells to form spheres when compared with the NC group.	Upregulation	HNE1, CNE1	Human	597
LINC00617	ENSG00000250366	lncRNA	26207516	2017	Long noncoding RNA LINC00617 exhibits oncogenic activity in breast cancer	breast cancer (BRCA)	With fluorescence activated cell sorter (FACS) analysis, we found that ectopic expression of linc00617 contributed to an increase in the percentage of the stem cell phenotype CD44high or CD24low subpopulation cells. Furthermore, LV-linc00617 transfected cells formed more and bigger mammospheres compared with vector-transfected cells. LINC00617, was upregulated in breast cancer samples. Knockdown of LINC00617 repressed lung metastasis in vivo. LINC00617 functions as an important regulator of EMT and promotes breast cancer progression and metastasis via activating the transcription of Sox2.	Upregulation	MCF7, T47D	Human	149
LINC02381	ENSG00000250742	lncRNA	35460500	2022	LINC02381-ceRNA exerts its oncogenic effect through regulation of IGF1R signaling pathway in glioma	glioma	LINC02381 was upregulation compared to normal tissues. Besides its expression was relatively stronger in invasive glioma cell lines. LINC02381 overexpression in the glioma cell lines induces the EMT phenotype and consequently increases the cell migration and stemness characteristics of the cells. LINC02381 exerts its oncogenic effect in glioma cells through sponging miR-128 and miR-150 to upregulate the IGF1R signaling pathway.	Upregulation	U87, 1321N1	Human	169
ZBED3-AS1	ENSG00000250802	lncRNA	34241580	2021	STAT3-induced ZBED3-AS1 promotes the malignant phenotypes of melanoma cells by activating PI3K or AKT signaling pathway	melanoma	ZBED3-AS1 expression was remarkably up-regulated in melanoma tissues. Loss-of-function assays verified that ZBED3-AS1 knockdown restrained cell proliferation, migration, epithelial-mesenchymal transition (EMT), and stemness in melanoma. ZBED3-AS1 promoted the malignant progression of melanoma by regulating miR-381-3p or ARID4B axis to activate the phosphatidylinositol 3-kinase or AKT serine or threonine kinase (PI3K or AKT) signalling pathway.	Upregulation	M21, SK-MEL-1	Human	643
MALAT1	ENSG00000251562	lncRNA	31012108	2019	Long noncoding RNA MALAT1 mediates stem cell-like properties in human colorectal cancer cells by regulating miR-20b-5p or Oct4 axis	colorectal carcinoma (CRC)	si-MALAT1 and miR-20b-5p-mimic attenuated microsphere formation and self-renewal capacity, decreased the proportion of CSCs, and downregulated the expression of proteins associated with tumor cell stemness maintenance (Oct4, Nanog, sex-determining region Y-box 2, and Notch1) and cellular metabolism (glucose transporter 1, lactate dehydrogenase B, hexokinase 2, and pyruvate kinase isozyme M2) in HCT-116 cells in vitro.	Upregulation	HCT-116	Human	198
MALAT1	ENSG00000251562	lncRNA	29202181	2018	Targeted nanocomplex carrying siRNA against MALAT1 sensitizes glioblastoma to temozolomide	glioblastoma (GBM)	MALAT1 was also significantly upregulated in 3D tumorsphere culture compared with 2D monolayer culture. The tumorsphere formation assay confirmed that targeting of MALAT1 via scL-siMAL significantly decreased the self-renewal capacity of T98G (43.5percentage reduction compared with that of untreated cells), while no significant inhibition of sphere formation was observed with the scL-siCTRL treatment. A similar level of inhibition of tumorsphere formation was observed in U87R cells. Attenuation of MALAT1 by RNA interference significantly lowered the growth, motility and stemness of GBM cells. In addition, silencing of MALAT1 clearly improved the sensitivity of GBM cells to chemotherapeutic agents.	Upregulation	U87, T98G	Human	199
MALAT1	ENSG00000251562	lncRNA	30500989	2019	Interaction of lncRNA-MALAT1 and miR-124 regulates HBx-induced cancer stem cell properties in HepG2 through PI3K or Akt signaling	hepatocellular carcinoma (HCC)	Overexpression of miR-124 or silencing of lncRNA-MALAT1 both blocked HBx-induced CSC generation, stemness-related factor activation and tumorigenicity via PI3K or Akt signaling.	Upregulation	HepG2	Human	200
MALAT1	ENSG00000251562	lncRNA	32626943	2020	lncRNA MALAT1 modulates cancer stem cell properties of liver cancer cells by regulating YAP1 expression via miR-375 sponging	liver cancer (HULC)	The expression level of MALAT1 was elevated in cancer spheroids compared with the corresponding levels noted in parental liver cancer cells, whereas the suppression of MALAT1 resulted in markedly reduced sphere formation and decreased expression of stemness factors in liver cancer cells. MALAT1 may promote CSC properties of liver cancer cells by upregulating YAP1 expression via sponging miR-375.	Upregulation	Huh7, HepG2	Human	201
MALAT1	ENSG00000251562	lncRNA	28615056	2017	Oct4 transcriptionally regulates the expression of long non-coding RNAs NEAT1 and MALAT1 to promote lung cancer progression	lung cancer (LC)	Lung cancer cells overexpressing NEAT1 or MALAT1 and the Oct4-silenced cells reconstituted with NEAT1 or MALAT1 promoted cell proliferation, migration and invasion. In addition, knockdown of NEAT1 or MALAT1 abolished Oct4-mediated lung cancer cell growth and motility.	Upregulation	A549, CL1-0	Human	202
MALAT1	ENSG00000251562	lncRNA	30481748	2018	LncRNA MALAT1 Promotes Cancer Metastasis in Osteosarcoma via Activation of the PI3K-Akt Signaling Pathway	osteosarcoma (OS)	MALAT1 was significantly up-regulated in osteosarcoma tissues compared with adjacent non-tumor soft tissues. In addition, the microsphere formation assay showed that MALAT1 overexpression significantly increased tumor microsphere formation, whereas MALAT1 knockdown significantly inhibited the number and size of tumor microspheres in both SW1353 and SOSP-9607 cells. MALAT1 increases stem cell-like properties by up-regulating RET via sponging miR-129-5p, and thus activates the PI3K-Akt signaling pathway.	Upregulation	SOSP-9607, SW1353	Human	203
MALAT1	ENSG00000251562	lncRNA	32433460	2020	The Long Non-Coding RNA MALAT1 Enhances Ovarian Cancer Cell Stemness by Inhibiting YAP Translocation from Nucleus to Cytoplasm	ovarian cancer (OC)	MALAT1 level was remarkably higher in non-adherent spheres formed by adherent ovarian cancer cells, as well as cisplatin-resistant ovarian cancer cells. MALAT1 knockdown reduced ovarian cancer cell stemness, characterized as the decrease of sphere forming ability, expression of stemness regulatory masters, and attenuation of cisplatin resistance.	Upregulation	SKOV3	Human	204
MALAT-1	ENSG00000251562	lncRNA	29434914	2018	Long non-coding RNA MALAT-1 contributes to maintenance of stem cell-like phenotypes in breast cancer cells	breast cancer (BRCA)	The expression of MALAT-1 was higher in the CSC subpopulation compared with that in the overall MCF7 cell group. The self-renewal assay also demonstrated that knockdown of MALAT-1 decreased the sphere formation rate in vitro. MALAT-1 is also able to regulate the proliferation, colony formation, migration and invasion of CSCs in vitro. MALAT-1 affects the stem cell-like phenotypes in breast cancer cells through regulation of Sox-2.	Upregulation	MCF7	Human	205
MALAT-1	ENSG00000251562	lncRNA	25811929	2015	Long noncoding RNA MALAT-1 enhances stem cell-like phenotypes in pancreatic cancer cells	pancreatic cancer (PaCa)	MALAT-1 was upregulated in CSCs and could increase the proportion of CSCs in pancreatic cancer cells. MALAT-1 Enhances Spheroid Forming Ability and Anchorage Independent Growth of Pancreatic Cancer Cells. Elevated Expression Levels of MALAT-1 in Pancreatic Cancer Cells Accelerate HUVEC Tube Formation and Migration. Downregulation of MALAT-1 Reduces Self-Renewal Associated Factors Expression of Pancreatic Cancer Cells.	Upregulation	AsPC-1, CFPAC-1	Human	206
HOXA10-AS	ENSG00000253187	lncRNA	33831733	2021	Promotive effects of HOXA10 antisense RNA on the stemness of oral squamous cell carcinoma stem cells through a microRNA-29a or MCL-1 or phosphatidyl inositol 3-kinase or protein kinase B axis	oral squamous cell carcinoma (OSCC)	HOXA10-AS and MCL-1 were highly expressed while miR-29a was poorly expressed in the collected tumor tissues and the extracted OSCC stem cells. Silencing of HOXA10-AS suppressed proliferation and tumor sphere formation ability of stem cells, and it reduced growth and metastasis of tumors in animals. HOXA10-AS enhances the stem cell property of OSCC stem cells through the miR-29a or MCL-1 or PI3K or AKT axis.	Upregulation	Tca8113	Human	116
TUG1	ENSG00000253352	lncRNA	32390141	2020	LncRNA TUG1 facilitates proliferation, invasion and stemness of ovarian cancer cell via miR-186-5p or ZEB1 axis	ovarian cancer (OC)	The silencing of TUG1 and upregulation of miR-186-5p both suppressed the cell proliferation, invasion and cancer stem cell (CSC) properties. TUG1 sponges miR-186-5p to release ZEB1 and promotes the proliferation, invasion and stemness of OC cells.	Upregulation	A2780, SKOV3	Human	638
PCAT1	ENSG00000253438	lncRNA	33277858	2020	GATA6 activated long non-coding RNA PCAT1 maintains stemness of non-small cell lung cancer by mediating FRK	non-small cell lung cancer (NSCLC)	PCAT1 was aberrantly elevated in tissues from patients with NSCLC. PCAT1 knockdown reduced cell proliferation, stem cell properties of H226 and A549 cells in vitro, and repressed tumor development in vivo. GATA6 or PCAT1 may markedly maintain the stemness of NSCLC, resulting in late TNM stage and poor survival.	Upregulation	H226, A549	Human	588
HOXA-AS2	ENSG00000253552	lncRNA	30412716	2019	Long non-coding RNA HOXA-AS2 promotes the migration, invasion and stemness of bladder cancer via regulating miR-125b or Smad2 axis	bladder cancer (BLCA)	We demonstrated the upregulation of HOXA-AS2 in both bladder cancer cells and clinical bladder tumors. After knockdown of HOXA-AS2 in bladder cancer 5637 and T24 cells, the migration, invasion and stemness of cancer cells were significantly inhibited, indicating the capability of HOXA-AS2 to promote the migration, invasion and stemness of bladder cancer cells. The involvement of HOXA-AS2 or miR-125b or Smad2 interactions in the functional role of HOXA-AS2 in mediating the migration, invasion and stemness of bladder cancer cells.	Upregulation	5637, T24	Human	121
HOXA-AS2	ENSG00000253552	lncRNA	33149607	2020	Integrated RNA Sequencing and Single-Cell Mass Cytometry Reveal a Novel Role of LncRNA HOXA-AS2 in Tumorigenesis and Stemness of Hepatocellular Carcinoma	hepatocellular carcinoma (HCC)	LncRNA HOXA-AS2 expression was significantly upregulated in HCC. A specific cancer stem cell subpopulation with EPCAM+, C-MYC+ and CK19+ may exist in higher HOXA-AS2 expression HCC patients.	Upregulation	THLE2	Human	122
LINC01419	ENSG00000253898	lncRNA	36050791	2022	The role of LINC01419 in regulating the cell stemness in lung adenocarcinoma through recruiting EZH2 and regulating FBP1 expression	lung adenocarcinoma (LUAD)	An up-regulation of LINC01419 level was demonstrated in LUAD cell lines and CD44 + LUAD cells. In LUAD cells, proliferation and stem cell sphere-formation that were attenuated by LINC01419 knockdown were discovered to be facilitated by LINC01419 overexpression.LINC01419, by recruiting EZH2 and regulating FBP1 expression, contributes to LUAD cell stemness.	Upregulation	A549, HCC78	Human	163
AGAP2-AS1	ENSG00000255737	lncRNA	33273726	2021	MSC-induced lncRNA AGAP2-AS1 promotes stemness and trastuzumab resistance through regulating CPT1 expression and fatty acid oxidation in breast cancer	breast cancer (BRCA)	Then, we investigated the effect of AGAP2-AS1 on stemness. RT-qPCR and western blot analyses verified that AGAP2-AS1 and the stemness genes were upregulated in BC cells upon the transfection of pcDNA3-1 or AGAP2-AS1. The proportion of CD44+ BC cells was also increased by AGAP2-AS1 overexpression. In addition, enhanced AGAP2-AS1 induced sphere formation and trastuzumab resistance of BC cells. However, when we silenced AGAP2-AS1 in BC cells co-cultured with MSCs, the MSC-culture caused stemness and trastuzumab resistance were dramatically abrogated. These results clearly indicate us that MSC caused stemness and trastuzumab resistance via inducing AGAP2-AS1.	Upregulation	SKBR-3, BT474	Human	5
TMPO-AS1	ENSG00000257167	lncRNA	34370878	2022	Long non-coding RNA TMPO-AS1 facilitates the progression of colorectal cancer cells via sponging miR-98-5p to upregulate BCAT1 expression	colorectal carcinoma (CRC)	TMPO-AS1 was aberrantly expressed at high levels in colorectal cancer cells. Silenced TMPO-AS1 restrained cell proliferation and stemness and promoted apoptosis oppositely. TMPO-AS1 promotes the progression of colorectal cancer cells via sponging miR-98-5p to upregulate BCAT1 expression.	Upregulation	HT-29, LOVO	Human	634
TMPO-AS1	ENSG00000257167	lncRNA	32988599	2020	LncRNA TMPO-AS1 Aggravates the Development of Hepatocellular Carcinoma via miR-429 or GOT1 Axis	hepatocellular carcinoma (HCC)	TMPO-AS1 expression was upregulated in HCC tissues and cell lines. The number of spheroids in Huh7 and SMMC-7721 cells was significantly decreased by TMPO-AS1 deficiency. TMPO-AS1 acted as a tumor motivator to expedite HCC progression via targeting miR-429 or GOT1 axis, which may provide a fresh treatment strategy for HCC.	Upregulation	Huh7, SMCC-7721	Human	635
LBX2-AS1	ENSG00000257702	lncRNA	33099720	2021	ELK1 activated-long noncoding RNA LBX2-AS1 aggravates the progression of ovarian cancer through targeting miR-4784 or KDM5C axis	ovarian cancer (OC)	LBX2-AS1 expression was markedly increased in OC tissues and cell lines. LBX2-AS1 silencing inhibited cell proliferation, migration and stemness but facilitated cell apoptosis in OC. Moreover, depletion of LBX2-AS1 suppressed tumor growth of OC in vivo.	Upregulation	CaOV3, SKOV3	Human	132
LINC00645	ENSG00000258548	lncRNA	31558707	2019	Long non-coding RNA LINC00645 promotes TGF-beta-induced epithelial-mesenchymal transition by regulating miR-205-3p-ZEB1 axis in glioma	glioma	LINC00645 expression was significantly upregulated in GBM tissues and cell lines. Knockdown of LINC00645 suppressed the proliferation, stemness, migration, invasion, and reversed transforming growth factor (TGF)-beta-induced motility of glioma cell lines. Subsequently, a significant decrease was detected in the volume and number of neurospheres transfected with si-linc 1_ compared with NC group, indicating that linc00645 play a role in GSCs. LINC00645 or miR-205-3p or ZEB1 signaling axis as a key player in EMT of glioma cells triggered by TGF-beta.	Upregulation	U251	Human	150
LINC-RoR	ENSG00000258609	lncRNA	35654242	2022	Functions of long non-coding RNA ROR in patient-derived glioblastoma cells	glioblastoma (GBM)	It is important to note that the highest level of linc-RoR was detected in 006 neurospheres, which, however, showed a relatively low expression of EGFR. In GBM cells LINC-RoR upregulates the levels of Sox2 and Oct4, and decreases the expression of p53. Therefore, LINC-RoR can allow GBM cells to maintain stemness by affecting these transcription factors.	Upregulation	glioblastoma cells	Human	173
ROR	ENSG00000258609	lncRNA	27602437	2016	Long Noncoding RNA ROR Regulates Proliferation, Invasion, and Stemness of Gastric Cancer Stem Cell	gastric cancer (GC)	LncRNA ROR was highly expressed in CD133+ GCSCs. Knockdown of lncRNA ROR inhibited the proliferation and invasion of GCSCs. ROR regulated the expression of several key stemness transcriptional factors.	Upregulation	MKN-45	Human	600
LINC00261	ENSG00000259974	lncRNA	35123494	2022	TGF-beta1 induced deficiency of LINC00261 promotes epithelial-mesenchymal-transition and stemness of hepatocellular carcinoma via modulating SMAD3	hepatocellular carcinoma (HCC)	LINC00261 was down-regulated in TGF-beta1 stimulated cells, and forced expression of LINC00261 attenuated EMT and stem-like traits in HCC. Further, linc00261 significantly inhibited the sphere formation in SMMC-7721 cells and Sk-hep1 LINC00261 suppressed EMT and stem-like traits in HCC cells by inhibiting TGF-beta1 or SMAD3 signaling.	Downregulation	SMMC-7721, Sk-hep-1	Human	142
NORAD	ENSG00000260032	lncRNA	34551785	2021	Long non-coding RNA NORAD promotes pancreatic cancer stem cell proliferation and self-renewal by blocking microRNA-202-5p-mediated ANP32E inhibition	pancreatic cancer (PaCa)	LncRNA NORAD and ANP32E were upregulated in PC tissues and cells, whereas the miR-202-5p level was down-regulated. Relative to the cells without treatment, the cells with miR-202-5p mimic or si-ANP32E exhibited a decreased proportion of ALDH high-activity cells, inhibited proliferation, accelerated apoptosis, increased G0 or G1 phase-arrested cells and decreased S phase-arrested cells, increased ratios of cleaved-caspase3 to pro-caspase3 and of cleaved-caspase9 to pro-caspase9, upregulated protein expression of PARP1, reduced colony and sphere formation, and downregulated expression of Oct4, Nanog and Sox2.	Upregulation	BxPC-3, MIAPaCa-2, PANC-1, HPDE6-C7	Human	584
DOCK9-AS2	ENSG00000260992	lncRNA	32917852	2020	Exosomal lncRNA DOCK9-AS2 derived from cancer stem cell-like cells activated Wnt or beta-catenin pathway to aggravate stemness, proliferation, migration, and invasion in papillary thyroid carcinoma	papillary thyroid carcinoma (PTC)	DOCK9-AS2 was upregulated in PTC, and presented elevation in plasma exosomes of PTC patients. PTC cells with DOCK9-AS2 knockdown presented restrained tumor sphere forming efficiency and lowered levels of stemness-related proteins including CD133, Nanog, OCT4, SOX2, EpCAM, and ALDH1A1. DOCK9-AS2 knockdown reduced proliferation, migration, invasion, epithelial-to-mesenchymal (EMT) and stemness in PTC cells. DOCK9-AS2 activated Wnt or beta-catenin pathway to aggravate PTC progression.	Upregulation	TPC1, BCPAP	Human	72
VPS9D1-AS1	ENSG00000261373	lncRNA	33627127	2021	Long non-coding RNA VPS9D1-AS1 facilitates cell proliferation, migration and stemness in hepatocellular carcinoma	hepatocellular carcinoma (HCC)	Up-regulated SEC61A1 facilitated cell proliferation, migration and stemness in HCC cells. Moreover, the migratory ability of HCC cells was impaired by the knockdown of SEC61A1. Sphere formation assay demonstrated that sphere formation efficiency was inhibited in SEC61A1 silenced HCC cells. MiR-491-5p negatively regulated SEC61A1 and inhibited HCC cell proliferation and migration by targeting SEC61A1.	Upregulation	HCCLM3, Huh-7	Human	640
LOXL1-AS1	ENSG00000261801	lncRNA	31468594	2019	LncRNA LOXL1-AS1 facilitates the tumorigenesis and stemness of gastric carcinoma via regulation of miR-708-5p or USF1 pathway	gastric cancer (GC)	LOXL1-AS1 was highly expressed in tissues and cells of gastric cancer. Sphere formation assay delineated that inhibition of LOXL1-AS1 significantly diminished the number and diameter of sphere. By contrast, ectopic expression of LOXL1-AS1 contributed to sphere-forming capability. LOXL1-AS1 accelerated the deterioration of gastric cancer by inducing cell proliferation, migration, EMT and stemness.	Upregulation	MKN-45, AGS	Human	191
LINC00662	ENSG00000261824	lncRNA	35551606	2022	LINC00662 enhances cell progression and stemness in breast cancer by MiR-144-3p or SOX2 axis	breast cancer (BRCA)	LINC00662 is overtly overexpressed in BC tissues and cell lines. We examined cell sphere numbers after knockdown of LINC00662 and found the number was decreased sharply, suggesting a decline in sphere formation efficiency. LINC00662 knockdown hampers cell proliferation, migration, invasion and stemness. LINC00662 enhances cell proliferation, migration, invasion and stemness in BC by targeting miR-144-3p or SOX2 axis.	Upregulation	MDA-MB-231, MCF-7	Human	151
LINC00662	ENSG00000261824	lncRNA	30256974	2018	Long non-coding RNA LINC00662 promotes cell invasion and contributes to cancer stem cell-like phenotypes in lung cancer cells	lung cancer (LC)	In the tumorsphere formation assay, the mammosphere number was significantly reduced in H1299 cells after the Linc00662 downregulation, and the mammosphere number was significantly increased in A549 cells after Linc00662 upregulation. The mammosphere number in tumorsphere formation assay was significantly lower in the si-Lin28 and pSin-Linc00662 co-transfected A549 cells than pSin-Linc00662 transfected A549 cells. Overexpression of LINC00662 enhances lung cancer cell metastasis and CSC stemness by interacting with Lin28 in human lung cancer.	Upregulation	H1299, A549	Human	152
FARSA-AS1	ENSG00000266975	lncRNA	33318478	2020	SOX9-activated FARSA-AS1 predetermines cell growth, stemness, and metastasis in colorectal cancer through upregulating FARSA and SOX9	colorectal carcinoma (CRC)	Importantly, knockdown of FARSA-AS1 markedly repressed the ability of SW480 and SW1116 cells to form primary, secondary, and tertiary spheres. Loss of FARSA-AS1 hindered malignant phenotypes in vitro and blocked tumor growth and metastasis in vivo. We testified that FARSA-AS1 aggravated the malignancy in CRC by enhancing SOX9 and FARSA.	Upregulation	SW480, SW1116	Human	79
ASB16-AS1	ENSG00000267080	lncRNA	34870557	2022	LncRNA ASB16-AS1 drives proliferation, migration, and invasion of colorectal cancer cells through regulating miR-185-5p or TEAD1 axis	colorectal carcinoma (CRC)	Then, we conducted sphere formation experiments to detect CRC cell stemness upon the ecotopic expression of ASB16-AS1. We discovered that the sphere formation efficiency was inhibited by ASB16-AS1 depletion, while it could be enhanced by ASB16-AS1 overexpression. After that, the expression of OCT4, Nanog, and SOX2, which were cell stemness markers was detected in CRC cells after ASB16-AS1 was silenced or overexpressed. The results uncovered that the expression of the above three markers was all decreased after ASB16-AS1 was silenced, while increased after ASB16-AS1 was overexpressed.	Upregulation	LOVO, HT-29	Human	8
ASB16-AS1	ENSG00000267080	lncRNA	32572790	2021	ASB16-AS1 up-regulated and phosphorylated TRIM37 to activate NF-kappaB pathway and promote proliferation, stemness, and cisplatin resistance of gastric cancer	gastric cancer (GC)	Then, we tested whether ASB16-AS1 regulated stem cell-like characteristics in GC cells. We observed that knocking down ASB16-AS1 declined tumor sphere formation efciency of GC cells. According to fow cytometry analysis, CD133+ GC cells presented a decreased ratio under ASB16-AS1 defciency.	Upregulation	MKN-45, HGC-27, MKN-7, GES-1	Human	9
FENDRR	ENSG00000268388	lncRNA	34697986	2021	Long non-coding RNA FENDRR inhibits the stemenss of colorectal cancer cells through directly binding to Sox2 RNA	colorectal carcinoma (CRC)	FENDRR level was remarkably lower in spheres formed by colorectal cancer cells compared to that in parental cancer cells. FENDRR overexpression attenuated the sphere-formation ability, ALDH activity and expression of stemness markers in colorectal cancer spheres. We found that FENDRR knockdown enhanced the sphere-formation capacity, as characterized by the increase of sphere number and size. FENDRR can block the CSC-like traits in colorectal cancer cells through directly interacting with Sox2 mRNA 3'UTR.	Downregulation	HCT-116, HT-29	Human	80
FENDRR	ENSG00000268388	lncRNA	30981768	2019	Long non-coding RNA FENDRR attenuates the stemness of non-small cell lung cancer cells via decreasing multidrug resistance gene 1 (MDR1) expression through competitively binding with RNA binding protein HuR	non-small cell lung cancer (NSCLC)	FENDRR expression was significantly decreased in NSCLC cells. We constructed NSCLC cells with FENDRR stable overexpression and revealed that FENDRR overexpression attenuated the stemness of NSCLC cells, evident by decreased stemness markers expression and capacity of cell spheroid formation. FENDRR attenuates NSCLC cell stemness through inhibiting the HuR or MDR1 axis.	Downregulation	NCIeH460, PC9, NCIeH292, NCIeH1975, A549, NCIeH1299, BEAS2B	Human	81
FOXF1-AS1	ENSG00000268388	lncRNA	27577075	2016	Loss of long noncoding RNA FOXF1-AS1 regulates epithelial-mesenchymal transition, stemness and metastasis of non-small cell lung cancer cells	non-small cell lung cancer (NSCLC)	The expression of FOXF1-AS1 was significantly downregulated in lung cancer,loss of FOXF1-AS1 mediates stem-like properties of lung cancer cells. The result showed that overexpression of FOXF1-AS1 significantly inhibits the sphere formation ability of CALU1 and NCIH1975 cells.	Downregulation	CALU1, NCIH1975	Human	88
SNHG8	ENSG00000269893	lncRNA	32538821	2020	LncRNA SNHG8 induces ovarian carcinoma cells cellular process and stemness through Wnt or beta-catenin pathway	ovarian cancer (OC)	Inhibition of SNHG8 executed suppressive activities in ovarian carcinoma by obstructing cell proliferation, migration, EMT process and stemness as well as driving cell apoptosis. SNHG8 acted as an oncogene in ovarian carcinoma via targeting Wnt or beta-catenin pathway.	Upregulation	SKOV3, CaOV3	Human	612
CASC15	ENSG00000272168	lncRNA	35235236	2022	LncRNA CASC15 regulates breast cancer cell stemness via the miR-654-5p or MEF2D axis	breast cancer (BRCA)	To assess the functional roles of CASC15 in BCSCs, the expression of stemness markers (OCT4, Nanog, and SOX2) in MCF-7 and T47D cells over-expressing CASC15 (oe-CASC15) was assessed. qRT-PCR revealed that the overexpression of CASC15 was directly proportional to that of stemness markers (OCT4, Nanog, SOX2) in MCF-7 and T47D cells. Flow cytometric analysis further revealed that higher CASC15 levels increased the differentiation of MCF-7 and T47D cells into CD44+ or CD24 phenotypes. Also, the colony formation ability of MCF-7 and T47D cells was increased by high levels of CASC15. Transfection of MCF-7 CSCs with si-CASC15 downregulated the expression of OCT4, Nanog, and SOX2 and generation of CD44+ CD24 cells from MCF-7 CSCs. Moreover, inhibition of CASC15 disrupted the spherification of MCF-7 CSCs. These findings suggest that CASC15 promotes the stemness of BCSCs.	Upregulation	MCF-7, T47D	Human	17
AFAP1-AS1	ENSG00000272620	lncRNA	34334630	2021	LncRNA AFAP1-AS1 or miR-27b-3p or VEGF-C axis modulates stemness characteristics in cervical cancer cells	cervical cancer (CC)	The present data confirmed that AFAP1-AS1 knockdown with its siRNAs (1-siAFAP1-AS1 and 2-siAFAP1-AS1) significantly suppressed the spheroid formation of CD44v6+ cells. Furthermore, AFAP1-AS1 siRNAs remarkably downregulated the expression of OCT4, OPN, and CD133 in the CD44v6+ cells.	Upregulation	SiHa, Hela	Human	2
AFAP1-AS1	ENSG00000272620	lncRNA	29971915	2018	Long non-coding RNA AFAP1-AS1 or miR-320a or RBPJ axis regulates laryngeal carcinoma cell stemness and chemoresistance	laryngeal carcinoma (LC)	To explore the role of AFAP1-AS1 in laryngeal carcinoma cell stemness, we performed qRT-PCR to detect AFAP1-AS1 expression between parental cells and stemness-enriched cell spheres. AFAP1-AS1 was significantly increased in cell spheres. To further explore AFAP1-AS1 function in laryngeal carcinoma cell development, we knocked down AFAP1-AS1 expression using siRNA transfection and confirmed silencing with qRT-PCR. We then used qRT-PCR to demonstrate that stemness-associated gene expression in the AFAP1-AS1-silenced cells was significantly reduced compared with control cells. Using tumour sphere assays, we then demonstrated that AFAP1-AS1 moderately inhibited cell self-renewal. Overall, these results suggest that AFAP1-AS1 contributes to laryngeal carcinoma tumorigenesis by promoting cancer cell stemness.	Upregulation	HEp-2	Human	3
AFAP1-AS1	ENSG00000272620	lncRNA	30819221	2019	Cross-talk among AFAP1-AS1, ACVR1 and microRNA-384 regulates the stemness of pancreatic cancer cells and tumorigenicity in nude mice	pancreatic cancer (PaCa)	Then, sphere formation and clone formation assays were performed, exhibiting fewer cell spheres, smaller microsphere diameter and lower monoclonal rate in the shRNA-AFAP1-AS1-1 and shRNA-AFAP1-AS1-2 groups than that in the shRNA-NC group, while the AFAP1-AS1 group showed opposite trend. Finally, EdU staining and Transwell assay revealed that the number of proliferative and migrated cells had diminished in the shRNA-AFAP1-AS1-1 and shRNA-AFAP1-AS1-2 groups compared with that in the control group, while the AFAP1-AS1 group showed opposite trend. Taken together, our findings demonstrated that AFAP1-AS1 could maintain stemness of pancreatic CSCs, while inhibition of AFAP1-AS1 exerted suppressive effects on sphere formation, proliferation, invasion and stemness of PC cells.	Upregulation	PANC-1, SW1990	Human	4
GAS6-AS2	ENSG00000272695	lncRNA	32799553	2021	GAS6-AS2 promotes Hepatocellular Carcinoma via miR-3619-5p or ARL2 Axis Under Insufficient Radiofrequency Ablation Condition	hepatocellular carcinoma (HCC)	GAS6-AS2 was upregulated in Huh7-H and MHCC97-H cells relative to Huh7 and MHCC97 cells. GAS6-AS2 deficiency hampered cell proliferation, migration, invasion, epithelial-mesenchymal transition, and stemness in Huh7-H and MHCC97-H cells. GAS6-AS2 served as the competing endogenous RNA (ceRNA) of ARL2 via absorbing miR-3619-5p.	Upregulation	HuH7, MHCC97	Human	90
DGCR5	ENSG00000273032	lncRNA	30980388	2019	DGCR5 promotes cancer stem cell-like properties of radioresistant laryngeal carcinoma cells by sponging miR-506 via Wnt pathway	human laryngeal carcinoma	DGCR5 was upregulated and microRNA-506 (miR-506) was downregulated in Hep-2R cells. Silence of DGCR5 could inhibit the stemness and enhance the radiosensitivity of Hep-2R cells. DGCR5 inhibition could repress Wnt signaling activity by sponging miR-506. In vivo assays were performed and we found that DCGR5 depressed stemness of human laryngeal cancer cells through modulating miR-506 and Wnt signaling pathway.	Downregulation	Hep-2, Hep-2R	Human	68
DGCR5	ENSG00000273032	lncRNA	29663359	2018	LncRNA DGCR5 contributes to CSC-like properties via modulating miR-330-5p or CD44 in NSCLC	non-small cell lung cancer (NSCLC)	We observed that DGCR5 was up-regulated in the enriched CSCs of NSCLC. DGCR5 can inhibit the stemness of NSLCL.	Downregulation	A549, H460, H1299	Human	69
DGCR5	ENSG00000273032	lncRNA	31920375	2019	lncRNA DGCR5 Up-Regulates TGF-beta1, Increases Cancer Cell Stemness and Predicts Survival of Prostate Cancer Patients	prostate cancer (PCa)	DGCR5 was down-regulated in tumor tissues than in adjacent healthy tissues of PC patients, but TGF-beta1 was up-regulated in the tumor tissues. DGCR5 over-expression led to decreased stemness of PC cells. DGCR5 may decrease the stemness of PC cells by down-regulating TGF-beta1.	Downregulation	22Rv1, DU145	Human	70
SNORD1C	ENSG00000274091	snoRNA	35422067	2022	SNORD1C maintains stemness and 5-FU resistance by activation of Wnt signaling pathway in colorectal cancer	colorectal carcinoma (CRC)	SNORD1C was upregulated in CRC and that high SNORD1C expression was related to poor prognosis. After knocking down SNORD1C in CRC cell lines, cell proliferation, colony formation, cell migration, and invasion were alleviated, while apoptosis was increased. SNORD1C functions via the Wnt or beta-catenin pathway to enhance cancer cell stemness in CRC.	Upregulation	SW620, HCT116	Human	614
LINC01232	ENSG00000280734	lncRNA	35026283	2022	FOXP3 activated-LINC01232 accelerates the stemness of non-small cell lung carcinoma by activating TGF-beta signaling pathway and recruiting IGF2BP2 to stabilize TGFBR1	non-small cell lung cancer (NSCLC)	LINC01232 expression was high in NSCLC cells. Finally, in sphere formation assay, we found that the sphere formation ability was significantly weakened by LINC01232 knockdown. FOXP3 activated-LINC01232 accelerated NSCLC cell stemness by activating TGF-beta signaling pathway and recruiting IGF2BP2 to stabilize TGFBR1.	Upregulation	NCI-H520, SK-MES-1	Human	159
CCAT2	ENSG00000280997	lncRNA	31904506	2020	Long non-coding RNA CCAT2 promotes oncogenesis in triple-negative breast cancer by regulating stemness of cancer cells	triple negative breast cancer (TNBC)	In view of the high degree of malignancy and high percentage of BCSCs in TNBC, cellular stemness assays were performed to determine whether CCAT2 regulates cancer stem cells in TNBC. Overexpression of CCAT2 induced the ALDH + cells with 4-fold more in MDA-MB-231 cells, and 3-fold more in MCF-10A-Src cells, than that in control cells. Mammosphere formation assay demonstrated increased sphere number and sphere diameter in CCAT2-overexpressing MDA-MB-231 cells under suspension culture condition. The gene expression analysis indicated the upregulation of those well-defined stemness markers including OCT4, NANOG and KLF4 at the mRNA levels. Validation of CCAT2 regulation of BCSCs was performed using sh-CCAT2. Knockdown of CCAT2 in MDA-MB-231 decreased the ratio of ALDH + cells from 1.6 percentage in control to 0.6 percentage in sh-CCAT2 cells. In consistence, decreased mRNA levels of OCT4, NANOG and KLF4 were demonstrated in the CCAT2 knockdown cells. Proteomic analysis confirmed the regulation of OCT4, NANOG and KLF4 at the protein levels by CCAT2 either overexpression or knockdown in MDA-MB-231 cells. Similar results in MCF-10A-Src cells.	Upregulation	MDA-MB-231, MCF-10A	Human	19
RBM5-AS1	ENSG00000281691	lncRNA	35110544	2022	Hypoxia-induced lncRNA RBM5-AS1 promotes tumorigenesis via activating Wnt or beta-catenin signaling in breast cancer	breast cancer (BRCA)	lncRNA RBM5-AS1 was remarkably upregulated in breast cancer cells and tissues. In addition, RBM5-AS1 overexpression elevated the sphere-forming efficiency (SFE), whereas RBM5-AS1-knockdown impaired the capacity for self-renewal in serial passaging. Overexpression of RBM5-AS1 facilitated proliferation, migration, invasion, EMT, and stemness maintenance of breast cancer cells in vitro and in vivo. RBM5-AS1 is a regulator of Wnt or beta-catenin signaling.	Upregulation	MCF-7, MDA-MB-231	Human	598
RBM5-AS1	ENSG00000281691	lncRNA	34225779	2021	RBM5-AS1 promotes radioresistance in medulloblastoma through stabilization of SIRT6 protein	medulloblastoma	Knockdown of RBM5-AS1 led to a reduction in the level of CD133 in radioresistant DAOY cells. RBM5-AS1 depletion decreased the expression of both CD44 and SOX2 in parental and radioresistant DAOY cells. Knockdown of RBM5-AS1 impaired the formation of spheres by radioresistant DAOY cells.	Upregulation	DAOY, D283Med	Human	599
LINC01606	ENSG00000282395	lncRNA	35485210	2022	Long noncoding RNA LINC01606 protects colon cancer (CC) cells from ferroptotic cell death and promotes stemness by SCD1-Wnt or beta-catenin-TFE3 feedback loop signalling	colon cancer (CC)	The expression of lncRNA LINC01606 was frequently upregulated in human colon cancer (CC) and strongly associated with a poor prognosis. As expected, the number of spheres formed was significantly inhibited in response to LINC01606 depletion, and conversely, LINC01606 overexpression significantly increased the tumour sphere number. LINC01606 functioned as an oncogene and promotes colon cancer (CC) cell growth, invasion and stemness both in vitro and in vivo.LINC01606 protected colon cancer (CC) cells from ferroptosis by decreasing the concentration of iron, lipid reactive oxygen species, mitochondrial superoxide and increasing mitochondrial membrane potential.	Upregulation	SW480, HT29	Human	166
MIR210HG	ENSG00000282810	lncRNA	34897892	2022	Hypoxia-inducible lncRNA MIR210HG interacting with OCT1 is involved in glioblastoma multiforme malignancy	glioblastoma (GBM)	A hypoxia-upregulated lncRNA, MIR210HG, locating in nuclear regions, predicted poor prognoses of patients and modulated hypoxia-promoted glioma stemness, TMZ resistance, and invasion.	Upregulation	U-87 MG, U-118 MG, PDM-123	Human	375
HULC	ENSG00000285219	lncRNA	35013529	2022	Induction of cancer cell stemness in glioma through glycolysis and the long noncoding RNA HULC-activated FOXM1 or AGR2 or HIF-1 alpha axis	liver cancer (HULC)	HULC was upregulated in GBM tissues and GSCs, which may promote the progression of glioma. Thus, the sh-HULC-1 silencing sequence was employed in subsequent experiments. Sphere formation assay results revealed a remarkably reduced number of GSC spheres following sh-HULC treatment. On the other hand, silencing of HULC reduced the stemness, inhibited the proliferation, and promoted the apoptosis and differentiation of GSCs. HULC promoted the glycolysis and stemness of GSCs through its regulation of the FOXM1 or AGR2 or HIF-1alpha axis, consequently exacerbating the occurrence and development of glioma.	Upregulation	U251	Human	126
H19	ENSG00000288237	lncRNA	29693231	2018	Lnc RNA H19 is associated with poor prognosis in breast cancer patients and promotes cancer stemness	breast cancer (BRCA)	In-vitro analysis showed that suppression of H19 using siRNA reduces sphere formation capacity in both HCC1934 and iCSCL10A cell lines. H19 was associated with stem cell phenotype in ALDH1-positive breast cancer.	Upregulation	HCC1934, iCSCL10A	Human	93
H19	ENSG00000288237	lncRNA	29106390	2018	Glycolysis gatekeeper PDK1 reprograms breast cancer stem cells under hypoxia	breast cancer (BRCA)	H19 knockdown decreases PDK1 expression in hypoxia, and ablation of PDK1 counteracts H19-mediated glycolysis and self-renewal ability in vitro and in vivo. Aspirin markedly attenuates glycolysis and cancer stem-like characteristics by suppressing both H19 and PDK1. In concordance, the mRNA level of H19 was also the highest expressing lncRNA in BCSC-enriched spheroid cells. In addition, there was a significant reduction in sphere sizes and numbers in MDA-MB-231-shH19 cells and MCF-7-shH19 cells.	Upregulation	MDA-MB-231, MCF-7	Human	94
H19	ENSG00000288237	lncRNA	32610610	2020	Enhancement of Breast Cancer Cell Aggressiveness by lncRNA H19 and its Mir-675 Derivative: Insight into Shared and Different Actions	breast cancer (BRCA)	A decrease of the sphere-forming capacity was observed in the native three cell lines when H19 was knocked down with siRNA, confirming that H19 was able to enhance the sphere-forming capacity of breast cancer cells. In vitro, H19 and miR-675 enhance the cell migration and invasion, as well as colony formation. H19 seems to induce the epithelial-to-mesenchymal transition (EMT), with a decreased expression of epithelial markers and an increased expression of mesenchymal markers.	Upregulation	MDA-MB-231, MCF-7	Human	95
H19	ENSG00000288237	lncRNA	30083271	2018	Carcinoma-associated fibroblasts promote the stemness and chemoresistance of colorectal cancer by transferring exosomal lncRNA H19	colorectal carcinoma (CRC)	H19 was highly expressed in the tumor tissues of CAC mice compared with the expression in normal colon tissues. The up-regulation of H19 was also confirmed in CRC patient samples at different tumor node metastasis (TNM) stages.The knockdown of H19 significantly decreased the sphere-propagating capacity, while the overexpression of H19 enhanced the sphere-propagating capacity in colon cancer (CC) cells (both SW480 and HCT116 cells). H19 promoted the stemness of CSCs and increased the frequency of tumor-initiating cells.CAFs promote the stemness and chemoresistance of CRC by transferring exosomal H19.	Upregulation	SW480, HCT116	Human	96
H19	ENSG00000288237	lncRNA	26274999	2016	Increased level of H19 long noncoding RNA promotes invasion, angiogenesis, and stemness of glioblastoma cells	hepatocellular carcinoma (HCC)	H19 was also significantly overexpressed in CD133+ glioblastoma cells, and overexpression of H19 was associated with increased neurosphere formation of glioblastoma cells. Increased expression of H19 lncRNA promotes invasion, angiogenesis, stemness, and tumorigenicity of glioblastoma cells.	Upregulation	U87, U373	Human	97
H19	ENSG00000288237	lncRNA	30410672	2018	H19 long non-coding RNA contributes to sphere formation and invasion through regulation of CD24 and integrin expression in pancreatic cancer cells	pancreatic ductal adenocarcinoma (PDAC)	The sphere-formation and invasion abilities of PDAC cells depended on H19 expression levels. The increased adhesion of H19-overexpressing cells was blocked by an anti-beta1-integrin antibody, and this resulted in the inhibition of sphere formation and invasion.	Upregulation	PANC-1, PK-59	Human	98
H19	ENSG00000288237	lncRNA	35565185	2022	Gp130-Mediated STAT3 Activation Contributes to the Aggressiveness of Pancreatic Cancer through H19 Long Non-Coding RNA Expression	pancreatic ductal adenocarcinoma (PDAC)	In H19-overexpressed PANC-1 sphere cells, the expression level of H19 was higher than that in mock-transfected sphere cells even after SC144-treatment. The reduction of MT1-MMP was also rescued in H19-overexpressed sphere cells. The 3D-invasion assay demonstrated that the reduction in invasion in SC144-treated mock-transfected PANC-1 sphere cells was partially rescued in H19-overexpressed sphere cells. H19, regulated by the gp130 or STAT3 pathway, partially contributes to EMT induction and invasion through MT1-MMP expression in PDAC CSC-like cells.	Upregulation	PANC-1	Human	99
H19	ENSG00000288237	lncRNA	30389909	2018	Estrogen receptor beta upregulated by lncRNA-H19 to promote cancer stem-like properties in papillary thyroid carcinoma	papillary thyroid carcinoma (PTC)	H19 is highly expressed in PTCSCs and PTC tissue specimens, which is correlated with poor overall survival. Silencing of H19 inhibits E2-induced sphere formation ability. Aspirin attenuates E2-induced cancer stem-like traits through decreasing both H19 and ERbeta expression.	Upregulation	TPC-1, K-1	Human	100
H19	ENSG00000288237	lncRNA	25567531	2015	Enrichment of Human Stem-Like Prostate Cells with s-SHIP Promoter Activity Uncovers a Role in Stemness for the Long Noncoding RNA H19	prostate cancer (PCa)	Targeted suppression of H19 with siRNA decreased Oct4 and Sox2 gene expression and colony-forming potential in RWPE-1 cells. Overexpression of H19 significantly increased gene expression of these two transcription factors and the sphere-forming capacity of RWPE-1 cells.	Upregulation	RWPE-1	Human	101
MCT-1	ENSG00000288295	lncRNA	31891569	2019	Multiple Copies in T-Cell Malignancy 1 (MCT-1) Promotes the Stemness of Non-Small Cell Lung Cancer Cells via Activating Interleukin-6 (IL-6) Signaling through Suppressing MiR-34a Expression	non-small cell lung cancer (NSCLC)	MCT-1 knockdown reduced the spheroid forming ability, characterized as the decreased spheroid size and number. MCT-1 knockdown decreased the expression of the NSCLC stemness markers and the activity of ALDH1. MCT-1 knockdown decreased IL-6 secretion that promotes NSCLC cell stemness. Furthermore, MCT-1 knockdown increased the level of miR-34a, which attenuated the stemness of NSCLC cells through targeting IL-6 receptor expression.	Upregulation	A549	Human	207
circ_0000291	hsa_circ_0000291	circRNA	35569812	2022	Circ_0000291 contributes to hepatocellular carcinoma tumorigenesis by binding to miR-1322 to up-regulate UBE2T	hepatocellular carcinoma (HCC)	Circ_0000291 knockdown also reduced the sphere formation efficiency of HCC cells. Western blot assays were conducted to measure the protein levels of proliferation-, apoptosis-, motility-, and sphere formation-associated markers (PCNA, Bax, Slug, and SOX2) in HCC cells. The data showed that circ_0000291 knockdown reduced the expression of PCNA, Slug, and SOX2 and increased the level of Bax in Huh-7 and LM6 HCC cells. These results showed that circ_0000291 knockdown suppressed the proliferation, migration, invasion, and stemness and induced the apoptosis of HCC cells.	Upregulation	Huh-7, LM6	Human	22
circ_0000745	hsa_circ_0000745	circRNA	34774079	2021	RNA-binding protein IGF2BP2 enhances circ_0000745 abundancy and promotes aggressiveness and stemness of ovarian cancer cells via the microRNA-3187-3p or ERBB4 or PI3K or AKT axis	ovarian cancer (OC)	Circ_0000745 and ERBB4 were abundantly expressed while miR-3187-3p was poorly expressed in OC tissues and cells. Circ_0000745 upregulated by IGF2BP2 promotes aggressiveness and stemness of OC cells through a miR-3187-3p or ERBB4 or PI3K or AKT axis.Again, inverse trends were found in SK-OV-3 cells where circ_0000745 was suppressed. The number of tumor spheres formed by ES-2 cells was increased whereas that by SK-OV-3 cells was reduced.	Upregulation	ES-2, SK-OV-3	Human	23
circ_0001535	hsa_circ_0001535	circRNA	36172827	2022	Circ_0001535 Facilitates Tumor Malignant Progression by miR-485-5p or LASP1 Axis in Colorectal Cancer	colorectal carcinoma (CRC)	Circ_0001535 was significantly upregulated in colorectal tissues and cells. Circ_0001535 knockdown suppressed the malignant behavior of colorectal cells such as proliferation, invasion, stemness, and tumor growth in vivo.	Upregulation	HCT116, SW480	Human	24
circ_0001550	hsa_circ_0001550	circRNA	35698305	2022	Hsa_circ_0001550 facilitates colorectal cancer progression through mediating microRNA-4262 or nuclear casein kinase and cyclin-dependent kinase substrate 1 cascade	colorectal carcinoma (CRC)	Hsa_circ_0001550 enrichment was enhanced in CRC tissue specimens and cell lines. Hsa_circ_0001550 depletion blocked CRC cell sphere formation efficiency. Hsa_circ_0001550 absence hindered CRC cell proliferation, metastasis, stemness, and caused apoptosis. Hsa_circ_0001550 facilitated CRC progression by binding to miR-4262 to positively regulate NUCKS1 abundance.	Upregulation	SW480, HCT116	Human	25
circ_0001666	hsa_circ_0001666	circRNA	34841662	2021	Hsa_circ_0001666 suppresses the progression of colorectal cancer through the miR-576-5p or PCDH10 axis	colorectal carcinoma (CRC)	Hsa_circ_0001666 was downregulated in both CRC cell lines along with tumour tissues. Hsa_circ_0001666 knockdown significantly supported CRC cell proliferation along with invasion and inhibited cell apoptosis in vitro. Then we performed a soft agar assay, and the results showed the number of spheres was significantly raised after hsa_circ_0001666 downregulation and decreased when PCDH10 was overexpressed.	Downregulation	LoVo, DLD-1	Human	26
circ_0003222	hsa_circ_0003222	circRNA	34433810	2021	hsa_circ_0003222 accelerates stemness and progression of non-small cell lung cancer by sponging miR-527	non-small cell lung cancer (NSCLC)	Hsa_circ_0003222 was highly expressed in NSCLC tissues and LCSCs. Cell proliferation was significantly higher when hsa_circ_0003222 was overexpressed and lower when the expression was inhibited. Similar results were obtained from colony and sphere formation. The silencing of hsa_circ_0003222 was found to downregulate PHF21B expression and its downstream, beta-catenin by relieving the sponging effect of miR-527. Moreover, silencing hsa_circ_0003222 alleviated NSCLC resistance to anti-programmed cell death-ligand 1 (PD-L1)-based therapy in vivo.	Upregulation	PC9, A549	Human	27
circKPNB1	hsa_circ_0004796	circRNA	35945192	2022	CircKPNB1 mediates a positive feedback loop and promotes the malignant phenotypes of GSCs via TNF-alpha or NF-kappaB signaling	glioma	CircKPNB1 was overexpressed in GBM and associated with GBM patients' poor prognosis. CircKPNB1 overexpression can promote the cell viabilities, proliferation, invasion, neurospheres formation abilities, and stemness of GSCs.	Upregulation	GSC28, GSC31, GSC32, GSC35, GSC38,GSC39	Human	49
circ_0006677	hsa_circ_0006677	circRNA	35081869	2022	Hsa_circ_0006677 regulates special AT-rich binding protein-2-mediated tumor-suppressive effect via functioning as a miR-1245a sponge in non-small cell lung cancer	non-small cell lung cancer (NSCLC)	We observed the downregulation of circ_0006677 in NSCLC samples and cells. Sphere formation assay displayed that the number of spheroids in the circ_0006677-overexpressing group was reduced significantly. Silencing of SATB2 was indeed able to re-establish the migrating and invading capacities, as well as the spheroid formation capacity of circ_0006677-overexpressing NSCLC cells.	Downregulation	H1299, A549	Human	28
circ_0007059	hsa_circ_0007059	circRNA	34847369	2022	Hsa_circ_0007059 sponges miR-421 to repress cell growth and stemness in hepatocellular carcinoma by the PTEN-AKT or mTOR pathway	hepatocellular carcinoma (HCC)	Circ_0007059 expression was downregulated in HCC samples and cells. Circ_0007059 overexpression inhibited HCC cell proliferation, migration, invasion, and stem cell-like property, and strengthened cell apoptosis. Circ_0007059 sponges miR-421 to inhibit oncogenic cellular process in HCC by mediating the PTEN-AKT or mTOR pathway.	Downregulation	SK-HEP1, MHCC97H	Human	29
circ_0007385	hsa_circ_0007385	circRNA	34989145	2022	Circ_0007385 regulates cell proliferation, apoptosis and stemness via targeting miR-493-3p or RAB22A axis in non-small cell lung cancer	non-small cell lung cancer (NSCLC)	Expression of circ_0007385 and RAB22A increased, whereas miR-493-3p level was decreased in NSCLC tissues in contrast to that in normal tissues. Circ_0007385 deficiency inhibited cell proliferation and stemness, whereas it promoted cell apoptosis in NSCLC cells. Circ_0007385 promoted NSCLC progression by sponging miR-493-3p to increase RAB22A expression.	Upregulation	A549, H1299	Human	30
circ_0007385	hsa_circ_0007385	circRNA	34620741	2022	Exosomal circ_0007385 enhances non-small cell lung cancer cell proliferation and stemness via regulating miR-1253 or FAM83A axis	non-small cell lung cancer (NSCLC)	Circ_0007385 was upregulated in NSCLC tissues and cells. Knockdown of circ_0007385 inhibited NSCLC cell proliferation and stemness. Moreover, cell sphere formation assay revealed that sphere formation efficiency was reduced by downregulating circ_0007385. Exosomal circ_0007385 promoted NSCLC cell proliferation and stemness by regulating miR-1253 or FAM83A axis.	Upregulation	A549, H1299	Human	31
circ_0026628	hsa_circ_0026628	circRNA	34420031	2021	Hsa_circ_0026628 promotes the development of colorectal cancer by targeting SP1 to activate the Wnt or beta-catenin pathway	colorectal carcinoma (CRC)	Circ_0026628 was upregulated in CRC cells. The sphere formation assay results disclosed that the number and size of spheres were both decreased and the relative sphere formation efficiency was also remarkably reduced in CRC cells with circ_0026628 depletion.	Upregulation	LOVO, SW480	Human	34
circ_0030167	hsa_circ_0030167	circRNA	33971282	2021	Exosomal circ_0030167 derived from BM-MSCs inhibits the invasion, migration, proliferation and stemness of pancreatic cancer cells by sponging miR-338-5p and targeting the Wif1 or Wnt8 or beta-catenin axis	pancreatic cancer (PaCa)	According to the qRT-PCR results, circ_0030167 was underexpressed in PANC-1 and MIA-PaCa-2 cancer cells. Coculture with exosomes and transfection of circ_0030167 significantly increased its abundance in PC cells. This molecule subsequently suppressed the proliferation, metastasis, and invasion of PC cells. Similarly, the stemness of PC cells was decreased to varying degrees.	Downregulation	PANC-1, MIA-PaCa-2	Human	35
circ_0030586	hsa_circ_0030586	circRNA	34175686	2021	Circ_0030586 inhibits cell proliferation and stemness in bladder cancer by inactivating the ERK signaling via miR-665 or NR4A3 axis	bladder cancer (BLCA)	The expression of circ_0030586 was significantly decreased in BCa tissues and cells, as suggested by RT-qPCR. A sphere formation assay revealed that the sphere forming capacity of BCa cells was significantly decreased due to circ_0030586 overexpression.	Downregulation	UMUC3, 5637	Human	36
circ_0044516	hsa_circ_0044516	circRNA	34258296	2021	Circ_0044516 Regulates miR-136 or MAT2A Pathway to Facilitate Lung Cancer Development	lung cancer (LC)	Circ_0044516 expression levels were obviously elevated in lung cancer tissues and cells. To study the function of circ_0044516 on lung cancer stem cell properties, spheroid formation assays were carried out and circ_0044516 siRNA decreased sphere numbers in A549 and SPCA1 cells.	Upregulation	A549, SPCA1	Human	37
circ-GSK3B	hsa_circ_0066903	circRNA	35821283	2022	Circ-GSK3B up-regulates GSK3B to suppress the progression of lung adenocarcinoma	lung adenocarcinoma (LUAD)	Circ-GSK3B was found to be significantly down-regulated in LUAD tissues and cells and it suppressed the proliferation, migration and stemness of LUAD cells. Moreover, the result of sphere formation assay demonstrated that the cell sphere formation efficiency was remarkably attenuated upon circ-GSK3B overexpression. Circ-GSK3B suppressed LUAD development through up-regulating and activating GSK3B.	Downregulation	H-1975, A549	Human	47
hsa-miR-29b-1	MI0000105	microRNA	25174983	2014	MicroRNA-29b-1 impairs in vitro cell proliferation, self-renewal and chemoresistance of human osteosarcoma 3AB-OS cancer stem cells	osteosarcoma (OS)	During the characterization of 3AB-OS cells, a CSC line selected from human OS MG63 cells, we showed a potent downregulation of miR-29b. Overall, the results show that miR-29b-1 suppresses stemness properties of 3AB-OS CSCs and suggest that developing miR-29b-1 as a novel therapeutic agent might offer benefits for OS treatment.	Downregulation	3AB-OS	Human	411
hsa-miR-34	MI0000268	microRNA	32717360	2020	A multimodal treatment of carbon ions irradiation, miRNA-34 and mTOR inhibitor specifically control high-grade chondrosarcoma cancer stem cells	chondrosarcomas (CSs)	Administration of a synthetic miR-34 mimic decreased sphere formation and invasion capabilities of CH-2879 ALDH+ cells, and increased ROS levels, indicating that the maintenance of chondrosarcoma stem-like phenotype may rely also on miR-34 repression.	Downregulation	CH-2879, OUMS27	Human	437
hsa-miR-34	MI0000268	microRNA	24009080	2013	Repression of c-Kit by p53 is mediated by miR-34 and is associated with reduced chemoresistance, migration and stemness	colorectal carcinoma (CRC)	Activation of a conditional miR-34a allele in DLD-1 cells diminished the expression of c-Kit and several stemness markers (CD44, Lgr5 and BMI-1) and suppressed sphere formation. MiR-34a also suppressed enhanced sphere-formation after exposure to SCF.	Downregulation	DLD-1	Human	438
hsa-miR-485	MI0002469	microRNA	30182373	2018	EGCG inhibits CSC-like properties through targeting miR-485 or CD44 axis in A549-cisplatin resistant cells	non-small cell lung cancer (NSCLC)	MiR-485 was greatly decreased in A549 or CDDP cells and miR-485 overexpression was able to decrease the stemness of A549 or DDP cells.	Downregulation	A549,A549 or CDDP	Human	503
hsa-let-7a	MIMAT0000062	microRNA	21292542	2011	MicroRNA let-7a represses chemoresistance and tumourigenicity in head and neck cancer via stem-like properties ablation	head and neck cancer (HNC)	We first demonstrated that let-7a expression was significantly decreased but that Nanog or Oct4 expression was increased in HNC tissues as compared to adjacent normal cells. The sphere-forming ability of ALDH1+ cells overexpressing let-7a or in which Nanog had been knocked down decreased after serial passaging. Expression of let-7a in recurrent HNC tissue and in regional metastatic lymph nodes of HNC patients was also significantly decreased, but Nanog or Oct4 expression was increased as compared to the expression levels in the parental tumours.	Downregulation	HNC	Human	133
hsa-let-7b	MIMAT0000063	microRNA	27520092	2016	Let-7b inhibits the malignant behavior of glioma cells and glioma stem-like cells via downregulation of E2F2	glioblastoma (GBM)	We found a significant decrease in the volume of tumor spheres 72 h after transfection of Let-7b mimics compared to the control group, which are consistent with the results that Let-7b has a negative effect on the proliferation of GSCs. The self-renewal ability of GSCs was measured by tumor sphere formation assay. Overexpression of Let-7b in GSCs led to a markedly decrease in their ability to form tumor spheres. Elevated levels of Let-7b resulted in a reduction of tumor sphere growth and stemness of glioma stem-like cells.	Downregulation	U251, U87	Human	134
hsa-let-7b-5p	MIMAT0000063	microRNA	34612147	2021	Silencing of let-7b-5p inhibits ovarian cancer cell proliferation and stemness characteristics by Asp-Glu-Ala-Asp-box helicase 19A	ovarian cancer (OC)	Let-7b-5p targeted DEAD (Asp-Glu-Ala-Asp)-box helicase 19A (DDX19A), which was downregulated in OVCA cells. A sphere formation assay revealed that knockdown of let-7b-5p markedly reduced the number of spheres, while transfection with MB-let-7b-5p inhibitor showed more significant inhibitory effects on the number of spheres. MB-let-7b-5p suppressed OVCA cell malignant behaviors by targeting DDX19A.	Upregulation	SKOV3, CAOV3	Human	135
hsa-let-7c	MIMAT0000064	microRNA	26420065	2015	PBX3 is targeted by multiple miRNAs and is essential for liver tumour-initiating cells	hepatocellular carcinoma (HCC)	We used the TIC-enriched Hep-12 and the non-tumorigenic Hep-11 cell lines by genome-wide profiling of miRNA expression with miRNA microarray analysis, followed by functional screening with soft-agar assay and we got let-7c, miR-200b, miR-222 and miR-424 which resulted in a complete inhibition of tumour formation. The spheroid formation efficiency decreased significantly when the expression of the four miRNAs was induced individually by DOX.	Downregulation	Hep-12, Huh7	Human	136
hsa-let-7c	MIMAT0000064	microRNA	29582468	2018	Let-7c restores radiosensitivity and chemosensitivity and impairs stemness in oral cancer cells through inhibiting interleukin-8	oral squamous cell carcinoma (OSCC)	The expression of let-7c in CSCs was reduced, while overexpression of let-7c attenuated the oncogenicity. Moreover, ectopic expression of let-7c in CSCs downregulated the stemness hallmarks and the radio or chemoresistance.	Downregulation	SAS, GNM	Human	137
hsa-let-7c-5p	MIMAT0000064	microRNA	35770722	2022	Withaferin A mediated changes of miRNA expression in breast cancer-derived mammospheres	breast cancer (BRCA)	WA-mediated miRNA expression, in particular, upregulation of miR-let-7c-5p, leads to the inhibition of breast cancer cells derived mammospheres. An increase in miR-let-7c-5p expression resulted in a decrease in the mRNA expression of CCND1 and c-MYC after WA treatment in both cell line-derived mammospheres.	Downregulation	MCF-7, T47D	Human	138
hsa-let-7d	MIMAT0000065	microRNA	31510100	2019	Differentially Expressed microRNAs in MIA PaCa-2 and PANC-1 Pancreas Ductal Adenocarcinoma Cell Lines are Involved in Cancer Stem Cell Regulation	pancreatic ductal adenocarcinoma (PDAC)	We report the miRNA expression characteristics of two cell lines, MIA PaCa-2 and PANC-1, and discovered three miRNAs (miR-7-5p, let-7d, and miR-135b-5p) that are involved in cancer stem cells (CSCs) suppression. After transfection of each miRNA's mimic into PANC-1 cells which exhibits higher stemness feature than MIA-PaCa-4 cells, partial reduction of CSC surface markers and inhibition of tumor sphere formation were observed.	Downregulation	MIA PaCa-2,PANC-1	Human	139
hsa-let-7e	MIMAT0000066	microRNA	31075231	2019	Induction of let-7e gene expression attenuates oncogenic phenotype in HCT-116 colorectal cancer cells through targeting of DCLK1 regulation	colorectal carcinoma (CRC)	Overexpression of let-7e effectively inhibited cell proliferation, suppressed migration, reduced sphere formation, and precluded EMT process as well as stemness factors. Let-7e plays an important role as tumor suppressor miRNA in CRC probably through inhibition of DCLK1 expression.	Downregulation	HCT-116	Human	140
hsa-miR-15a-5p	MIMAT0000068	microRNA	33273726	2021	MSC-induced lncRNA AGAP2-AS1 promotes stemness and trastuzumab resistance through regulating CPT1 expression and fatty acid oxidation in breast cancer	breast cancer (BRCA)	By generating miR-15a-5p mimics, we observed that miR-15a-5p significantly suppressed stemness and increased trastuzumab-mediated cytotoxicity.	Downregulation	SKBR-3, BT474	Human	307
hsa-miR-15a-5p	MIMAT0000068	microRNA	29164582	2017	miR-15a-5p suppresses endometrial cancer cell growth via Wnt or beta-catenin signaling pathway by inhibiting WNT3A	endometrial cancer (EC)	MiR-15a-5p was decreased in endometrial cancer cells and tissues. MiR-15a-5p overexpression restrained HEC-1-A cell proliferation and stemness. MiR-15a-5p is a regulator of endometrial cancer cell proliferation by directly targeting Wnt3a to block Wnt signaling pathway.	Downregulation	HEC-1-A	Human	308
hsa-miR-15a-5p	MIMAT0000068	microRNA	34365839	2021	ONECUT2 which is targeted by hsa-miR-15a-5p enhances stemness maintenance of gastric cancer stem cells	gastric cancer (GC)	We demonstrated significant overexpression of ONECUT2 and down-regulation of hsa-miR-15a-5p in gastric cancer. First, the results of stem cell sphere formation assay demonstrated that overexpression of hsa-miR-15a-5p could significantly inhibit the proliferation of GCSCs, that is, simultaneously inhibit the number and diameter of GCSCs spheres (p < 0.5). Hsa-miR-15a-5p regulates the stemness maintenance, epithelial-mesenchymal transition, and chemosensitivity of GCSCs through targeting ONECUT2. Also, hsa-miR-15a-5p inhibits G0 phase block of GCSCs by regulating ONECUT2 or beta-catenin signaling pathway.	Downregulation	MKN45	Human	309
hsa-miR-15a-5p	MIMAT0000068	microRNA	32398664	2020	CircZNF609 enhances hepatocellular carcinoma cell proliferation, metastasis, and stemness by activating the Hedgehog pathway through the regulation of miR-15a-5p or 15b-5p and GLI2 expressions	hepatocellular carcinoma (HCC)	Similarly, GLI2 upregulation or miR-15a-5p or 15b-5p suppression recovered circZNF609 depletion-mediated inhibitive effect on cell sphere formation ability to different degrees. CircZNF609 enhances HCC cell proliferation, metastasis, and stemness by activating the Hedgehog pathway through the regulation of miR-15a-5p or 15b-5p and GLI2 expressions.	Upregulation	HCCLM3, MHCC-97H	Human	310
hsa-miR-18	MIMAT0000072	microRNA	35416122	2022	MicroRNA-18 facilitates the stemness of gastric cancer by downregulating HMGB3 though targeting Meis2	gastric cancer (GC)	The stemness markers (ALDH1A1, SOX2, OCT4) expression was upregulated in miR-18 overexpressed cells, quantity of spheres were increased in miR-18-overexpressed cells. The CD44+ subpopulation with the stemness characteristics was increased by miR-18 overexpression. Tumors sprung from miR-18-overexpressed cells performed a significant increase of formation rate. Overexpression of miR-18 resulted in some extent of resistance to cisplatin.	Upregulation	AGS, MKN45	Human	312
hsa-miR-19a	MIMAT0000073	microRNA	29575299	2018	The PLGF or c-MYC or miR-19a axis promotes metastasis and stemness in gallbladder cancer	gallbladder cancer (GBC)	PLGF promotes EMT and tumorsphere formation through inducing miR-19a expression by upregulating c-MYC.	Upregulation	NOZ, GBC-SD	Human	332
hsa-miR-19a	MIMAT0000073	microRNA	28431267	2017	miR-19 targeting of GSK3beta mediates sulforaphane suppression of lung cancer stem cells	lung cancer (LC)	Overexpression of miR-19a or 19b enhanced the ability of tumorsphere formation, up-regulated the expression of lung CSCs markers, increased Wnt or beta-catenin pathway activation and beta-catenin or TCF transcriptional activity in lung CSCs. MiR-19 activated Wnt or beta-catenin pathway by directly targeting GSK3beta, the key negative modulator of this pathway.	Upregulation	A549, H1299	Human	333
hsa-miR-19b	MIMAT0000074	microRNA	34520626	2022	Exosomal microRNA-19b targets FBXW7 to promote colorectal cancer stem cell stemness and induce resistance to radiotherapy	colorectal carcinoma (CRC)	It was found that miR-19b was overexpressed in CRC tissues, which indicated a poor prognosis. It was also found that CRC-EXOs significantly enhanced sphere formation, while downregulation of miR-19b suppressed sphere formation. CRC-derived exosomes (EXOs) enhanced the radio-resistance and stemness properties of CRC cells via delivery of miR-19b in vitro and in vivo.	Upregulation	HCT116, DLD1	Human	334
hsa-miR-19b	MIMAT0000074	microRNA	28431267	2017	miR-19 targeting of GSK3beta mediates sulforaphane suppression of lung cancer stem cells	lung cancer (LC)	Overexpression of miR-19a or 19b enhanced the ability of tumorsphere formation, up-regulated the expression of lung CSCs markers, increased Wnt or beta-catenin pathway activation and beta-catenin or TCF transcriptional activity in lung CSCs. MiR-19 activated Wnt or beta-catenin pathway by directly targeting GSK3beta, the key negative modulator of this pathway.	Upregulation	A549, H1299	Human	335
hsa-miR-21	MIMAT0000076	microRNA	26314961	2015	STAT3 pathway regulates lung-derived brain metastasis initiating cell capacity through miR-21 activation	brain metastases (BM)	MiR-21 is overexpressed in lung cancer patients and predicts poor survival. Knockdown of miR-21 as confirmed by RT-PCR resulted in reduced BMIC proliferation , self-renewal and cell migration. Overexpression of miR -21 increases BMIC self-renewal and proliferation. MiR-21 knockdown corresponded with decreased sphere formation.	Upregulation	BT478, BT530	Human	366
hsa-miR-21	MIMAT0000076	microRNA	28121625	2017	Cancer-associated fibroblasts release exosomal microRNAs that dictate an aggressive phenotype in breast cancer	breast cancer (BRCA)	Differential expression profile analysis identified three miRs (miRs -21, -378e, and -143) increased in exosomes from CAFs as compared from normal fibroblasts. Normal fibroblast exosomes transfected with miRs -21, -378e, and -143 promoted the stemness and EMT phenotype of breast cancer cells.	Upregulation	T47D, BT549, MDA-MB-231	Human	367
hsa-miR-21	MIMAT0000076	microRNA	22435731	2012	MiR-21 regulates epithelial-mesenchymal transition phenotype and hypoxia-inducible factor-1alpha expression in third-sphere forming breast cancer stem cell-like cells	breast cancer (BRCA)	Both of HIF-1alpha and miR-21 were upregulated in the CSC-like cells. Antagonism of miR-21 significantly decreased the mammosphere forming efficiency (MSFE) of bCSC-like cells (P<0.0001). Interestingly, antagonism of miR-21 by antagomir led to reversal of EMT, downexpression of HIF-1alpha, as well as suppression of invasion and migration, which indicates a key role of miR-21 involved in regulate CSC-associated features.	Upregulation	MCF-7	Human	368
hsa-miR-21	MIMAT0000076	microRNA	22072622	2012	MicroRNA-21 induces stemness by downregulating transforming growth factor beta receptor 2 (TGFbetaR2) in colon cancer (CC) cells	colon cancer (CC)	The levels of beta-catenin, TCF or LEF activity and the expression of c-Myc, Cyclin-D, which are increased in CSCs, are also augmented in miR-21 overexpressing colon cancer (CC) cells, accompanied by an increased sphere forming ability in vitro and tumor formation in SCID mice.	Upregulation	HCT-116, HT-29	Human	369
hsa-miR-21	MIMAT0000076	microRNA	34314629	2022	Overexpression of circRNA circFAT1 in Endometrial Cancer Cells Increases Their Stemness by Upregulating miR-21 Through Methylation	endometrial cancer (EC)	Cell stemness assay was performed to investigate the role of circFAT1 and miR-21 in regulating the stemness of both RL95-2 and HEC-1-A cells. The percentage of CD133+ cells represents cell stemness. The results showed that overexpression of circFAT1 and miR-21 increased cell stemness, and inhibitor of miR-21 decreased cell stemness.Moreover, inhibitor of miR-21 reduced the effects of overexpression of circFAT1 on cell stemness	Upregulation	RL95-2, HEC-3-A	Human	370
hsa-miR-21	MIMAT0000076	microRNA	27644439	2016	Bmi-1 regulates stem cell-like properties of gastric cancer cells via modulating miRNAs	gastric cancer (GC)	The results showed that miR-21 expression in suspension microspheres which enrich stem-like cells increased significantly than in the parent adherent cells. MiR-21 upregulation can increase the microsphere formation rate, resistance to chemotherapy, and migration ability of gastric cancer cells, while miR-21 downregulation can decrease the microsphere formation rate, resistance to chemotherapy, and migration ability. Bmi-1 positively regulates stem cell-like properties via upregulating miR-21, and miR-34a negatively regulates stem cell-like characteristics by negative feedback regulation of Bmi-1 in gastric cancer.	Upregulation	SGC7901	Human	371
hsa-miR-21	MIMAT0000076	microRNA	23890123	2013	MicroRNA-21 promotes the ovarian teratocarcinoma PA1 cell line by sustaining cancer stem or progenitor populations in vitro	ovarian teratocarcinoma (OVTC)	Knockdown of miR-21 resulted in a marked reduction in the CD133+ population and sphere formation of CSPCs. Overexpression of miR-21 resulted in a marked increase in the population of CD133+ cells as well as sphere formation of CSPCs.	Upregulation	PA1, HEK293T	Human	372
hsa-miR-21	MIMAT0000076	microRNA	35163198	2022	microRNA-21 Regulates Stemness in Pancreatic Ductal Adenocarcinoma Cells	pancreatic ductal adenocarcinoma (PDAC)	MiR-21 was highly expressed in Panc-1 and MiaPaCa-2 PDAC cells in association with CSCs. MiR-21 knockouts from both MiaPaCa-2 and Panc-1 cell lines, reversed expressions of epithelial-mesenchymal transition (EMT) and CSCs markers were observed. MiR-21 (KO) suppressed cellular invasion and proliferation of Panc-1 and MiaPaCa-2 cells.	Upregulation	MiaPaCa-2, Panc-1	Human	373
hsa-miR-21-5p	MIMAT0000076	microRNA	34694765	2021	MiR-21-5p inhibition attenuates Warburg effect and stemness maintenance in osteosarcoma cells via inactivation of Wnt or beta-catenin signaling	osteosarcoma (OS)	MiR-21-5p inhibition suppressed tumorsphere for- mation of MG-63 cells. The effect of miR-21-5p suppression on stemness and the Warburg effect may be associated with the decreased activity of the Wnt or beta-catenin pathway in OS cells.	Upregulation	MG-63	Human	380
hsa-miR-21-5p	MIMAT0000076	microRNA	33728488	2022	microRNA-21-5p from M2 macrophage-derived extracellular vesicles promotes the differentiation and activity of pancreatic cancer stem cells by mediating KLF3	pancreatic cancer (PaCa)	MiR-21a-5p was upregulated in M2 macrophage-derived EVs. MiR-21a-5p downregulation in M2 macrophage-derived EVs inhibited Nanog or Oct4 expression and impaired sphere-forming, colony-forming, invasion, migration, and anti-apoptosis abilities of PaCa stem cells in vitro and tumorigenic ability in vivo. MiR-21-5p targeted KLF3 to mediate the differentiation and activities of PaCa stem cells, and KLF3 was downregulated in PaCa stem cells.	Upregulation	AsPC-1, PANC-1	Human	381
hsa-miR-22-3p	MIMAT0000077	microRNA	34019487	2021	Chronic alcohol exposure promotes HCC stemness and metastasis throughbeta-catenin or miR-22-3p or TET2 axis	hepatocellular carcinoma (HCC)	MiR-22-3p promotes stemness and metastasis of HCC through TET2. In the tumorspheres culture assay, the size and number of tumorspheres in miR-22-3p-overexpressed HCC cells were greater than those of the control group, while the miR-22-3p inhibition showed an opposite effect.	Upregulation	HepG2, SMMC-7721	Human	397
hsa-miR-25	MIMAT0000081	microRNA	30868061	2019	SLC34A2 promotes neuroblastoma cell stemness via enhancement of miR-25 or Gsk3beta-mediated activation of Wnt or beta-catenin signaling	neuroblastoma	SLC34A2 facilitates the stemness of SH-SY5Y cells at least through the miR-25-Gsk3beta axis. MiR-25 or Gsk3beta-mediated activation of Wnt signaling is responsible for SLC34A2-induced enhancement of neuroblastoma cell stemness.	Upregulation	SH-SY5Y	Human	399
hsa-miR-26b-5p	MIMAT0000083	microRNA	34802869	2022	Gamma-mangostin isolated from garcinia mangostana suppresses colon carcinogenesis and stemness by downregulating the GSK3beta or beta-catenin or CDK6 cancer stem pathway	colorectal carcinoma (CRC)	Pharmacological intervention with gMG suppressed CRC carcinogenesis and stemness via downregulating GSK3 or beta-catenin or CDK6 and upregulating the miR-26b-5p tumor suppressor.	Downregulation	HCT116, HT29	Human	400
hsa-miR-26b-5p	MIMAT0000083	microRNA	31276277	2019	miR-26b-5p helps in EpCAM+cancer stem cells maintenance via HSC71 or HSPA8 and augments malignant features in HCC	hepatocellular carcinoma (HCC)	MiR-26b-5p imparts metastatic properties and helps in maintenance of Ep+ CSCs via HSPA8. Reduced miR-26b-5p expression increased the spheroid formation, migration, invasion and tumourigenicity of Ep+ CSCs.	Downregulation	HuH7, HepG2	Human	401
hsa-miR-27a-3p	MIMAT0000084	microRNA	34601333	2021	Exosomes secreted by M2 macrophages promote cancer stemness of hepatocellular carcinoma via the miR-27a-3p or TXNIP pathways	hepatocellular carcinoma (HCC)	MiR-27a-3p was upregulated and TXNIP was downregulated in HCC cells, and M2 exosomes further upregulated miR-27a-3p. The upregulated M2 exosomal miR-27a-3p promoted stemness, proliferation, drug resistance, migration, invasion and in vivo tumorigenicity of HCC cells. M2 macrophages-derived exosomal miR-27a-3p promotes cancer stemness of HCC via downregulating TXNIP.	Upregulation	SMMC-7721	Human	402
hsa-miR-30a-5p	MIMAT0000087	microRNA	33023006	2020	STAT3 Mediated miR-30a-5p Inhibition Enhances Proliferation and Inhibits Apoptosis in Colorectal Cancer Cells	colorectal carcinoma (CRC)	A comparison of small RNAseq results between tumorspheres and HT29shSTAT3 cells revealed miR-30a-5p was downregulated. A STAT3-miR-30a-5p-HSPA5 axis was observed against regorafenib-mediated apoptosis in colorectal cancer tumorspheres.	Downregulation	HCT116, HT29	Human	420
hsa-miR-33a	MIMAT0000091	microRNA	35579082	2022	CircPCBP2 promotes the stemness and chemoresistance of DLBCL via targeting miR-33a or b to disinhibit PD-L1	diffuse large B-cell lymphoma (DLBCL)	CircPCBP2 was upregulated in human DLBCL specimens and cultured DLBCL cells while miR-33a or b was reduced. Knockdown of circPCBP2 or miR-33a or b overexpression inhibited the stemness of DLBCL cells and promoted cancer cell apoptosis upon CHOP treatment. CircPCBP2 enhances DLBCL cell stemness but suppresses its sensitivity to CHOP via sponging miR-33a or b to disinhibit PD-L1 expression.	Downregulation	U2932, OCI-LY3, SU-DHL-3, NU-DUL-1	Human	434
hsa-miR-92	MIMAT0000092	microRNA	28209618	2017	The STAT3-miRNA-92-Wnt Signaling Pathway Regulates Spheroid Formation and Malignant Progression in Ovarian Cancer	epithelial ovarian cancer (EOC)	STAT3-induced miR-92a expression is required for spheroid formation and tumor growth. To further validate the functional role of miR-92a in ovarian cancer spheroids, we determined the spheroid formation in STAT3-KD cells and found that the decreased spheroid formation by STAT3 inhibition was recovered by overexpression of miR-92a. STAT3 signaling maintained stemness and interconnected Wnt or beta-catenin signaling via the miR-92a or DKK1-regulatory pathways.	Upregulation	SKOV3, HeyA8	Human	567
hsa-miR-92a	MIMAT0000092	microRNA	35184640	2022	Knockdown of miR-92a suppresses the stemness of colorectal cancer cells via mediating SOCS3	colorectal carcinoma (CRC)	SOCS3 was lowly expressed while miR-92a was highly expressed in CRC. By using two CRC CSC cell lines (SW480 and LoVo) treated with the miR-92a inhibitor or matched inhibitor NC, we found that miR-92a inhibition markedly repressed the sphere formation ability. MiR-92a inhibition remarkably suppressed self-renewal and growth of CSC cells.	Upregulation	LoVo, SW480	Human	568
hsa-miR-92a-3p	MIMAT0000092	microRNA	31064356	2019	CAFs secreted exosomes promote metastasis and chemotherapy resistance by enhancing cell stemness and epithelial-mesenchymal transition in colorectal cancer	colorectal carcinoma (CRC)	miR-92a-3p expression is significantly increased in CRC tissues. Increased expression of miR-92a-3p activates Wnt or beta-catenin pathway and inhibits mitochondrial apoptosis by directly inhibiting FBXW7 and MOAP1, contributing to cell stemness, EMT, metastasis and 5-FU or L-OHP resistance in CRC.	Upregulation	NCM460	Human	569
hsa-miR-92a-3p	MIMAT0000092	microRNA	27801803	2016	miR-92a-3p Exerts Various Effects in Glioma and Glioma Stem-Like Cells Specifically Targeting CDH1 or beta-Catenin and Notch-1 or Akt Signaling Pathways	glioma	We observed that up-regulation of miR-92a-3p could inhibit the stemness of GSCs.	Downregulation	U87, U251	Human	570
hsa-miR-93	MIMAT0000093	microRNA	29110645	2017	Long intergenic non-protein-coding RNA 1567 (LINC01567) acts as a sponge against microRNA-93 in regulating the proliferation and tumorigenesis of human colon cancer (CC) stem cells	colon cancer (CC)	MiR-93 and Musashi-1 mediated the tumor suppression of LOCCS knockdown. There was reciprocal repression between LOCCS and miR-93.	Downregulation	SW1116	Human	571
hsa-miR-96	MIMAT0000095	microRNA	27431799	2016	MicroRNA-183 suppresses cancer stem-like cell properties in EBV-associated nasopharyngeal carcinoma	nasopharyngeal carcinoma (NPC)	Downregulation of miR-96 and miR-183 was confirmed in NPC spheroids. That ectopic expression of miR-96 and miR-183 suppressed cell growth and tumor sphere formation in NPC. The tumorigenicity of cells stably expressing miR-184 was significantly inhibited in the in vivo nude mice model.	Downregulation	C666-1	Human	574
hsa-miR-98-5p	MIMAT0000096	microRNA	33798550	2021	miR-98-5p inhibits gastric cancer cell stemness and chemoresistance by targeting branched-chain aminotransferases 1	gastric cancer (GC)	MiR-98 was decreased in CD44+ GCSCs. The overexpression of miR-98 could inhibit the expression of stem-related genes and the ability of self-renewal, invasion, and tumorigenicity of GCSCs. MiR-98 inhibits gastric cancer cell stemness and chemoresistance by targeting BCAT1.	Downregulation	BGC-823, SNU-16	Human	576
hsa-miR-99a	MIMAT0000097	microRNA	29072692	2017	miR-99a reveals two novel oncogenic proteins E2F2 and EMR2 and represses stemness in lung cancer	lung cancer (LC)	By inhibiting E2F2 and EMR2, miR-99a represses in vivo the transition of epithelial cells through an EMT process concomitantly with the inhibition of stemness features and consequently decreasing the CSC population.	Downregulation	H1975, H1299	Human	577
hsa-miR-99a	MIMAT0000097	microRNA	32199224	2020	Transcriptional factor Yin Yang 1 facilitates the stemness of ovarian cancer via suppressing miR-99a activity through enhancing its deacetylation level	ovarian cancer (OC)	MiR-99a negatively regulates the stemness of OC cells. The sphere size and number were remarkably decreased or increased by miR-99a overexpression or knockdown. Overexpression of miR-99a or knockdown of HDAC5 attenuated the promoting effects of YY1 on the stemness of OC cells.	Downregulation	HO8910, SKOV3	Human	578
hsa-miR-100	MIMAT0000098	microRNA	24805183	2014	Loss of miR-100 enhances migration, invasion, epithelial-mesenchymal transition and stemness properties in prostate cancer cells through targeting Argonaute 2	prostate cancer (PCa)	MiR-100 is downregulated in human prostate cancer tissue compared to normal prostate and also significantly decreased in bone metastatic prostate cancer samples compared with primary prostate cancer. Downregulation of AGO2(the core effector protein of the miRNA-induced silencing)enhanced expression of miR-34a and miR-125b which can suppress migration, invasion, EMT and stemness of cancer cells.	Upregulation	PC-3, DU145	Human	208
hsa-miR-29b	MIMAT0000100	microRNA	26155940	2015	miR-29b attenuates tumorigenicity and stemness maintenance in human glioblastoma multiforme by directly targeting BCL2L2	glioblastoma (GBM)	MiR-29b inhibits angiogenesis by attenuating tube formation and the expression of VEGF and Ang-2, and stemness maintenance in GBM cells, as demonstrated by decreasing neurosphere formation and cancer stem cell marker protein expression.	Downregulation	U251, U87	Human	409
hsa-miR-29b	MIMAT0000100	microRNA	29119708	2018	Eukaryotic Initiation Factor 5A2 Contributes to the Maintenance of CD133+ Hepatocellular Carcinoma Cells via the c-Myc or microRNA-29b Axis	hepatocellular carcinoma (HCC)	Downregulated miR-29b level is responsible for EIF5A2-maintained HCC cell stemness either in vitro or in vivo. EIF5A2 contributes to the maintenance of CD133+ HCC cells via the c-Myc or miR-29b axis.	Downregulation	PLC8024, Huh7	Human	410
hsa-miR-103	MIMAT0000101	microRNA	31273221	2019	miR-103 or 107 prolong Wnt or beta-catenin signaling and colorectal cancer stemness by targeting Axin2	colorectal carcinoma (CRC)	Again, miR-103 or 107 overexpression led to a significant increase in the formation of secondary spheres. MiR-103 or 107 stimulate multiple stem-like features in colorectal cancer, including expression of stem-like markers, appearance of side-population cells, and capabilities in self-renewal, tumor initiation, recurrence, and chemoresistance. MiR-103 or 107 in promoting colorectal cancer stemness by targeting Axin2.	Upregulation	HCT116	Human	209
hsa-miR-103a	MIMAT0000101	microRNA	34905060	2022	Targeting radiation-tolerant persister cells as a strategy for inhibiting radioresistance and recurrence in glioblastoma	glioblastoma (GBM)	Restoring miR-103a expression under these conditions suppressed the FGF2-XRCC3 axis and decreased the radioresistance capability. Subsequently, we demonstrated that ectopic expression of miR-103a significantly reduced GSC tumorsphere formation. MiR-103a suppresses stemness in the RTP subset by targeting FGF2, which is downstream of miR-103a and involved in DNA damage repair in RTP cells via the NHEJ pathway.	Downregulation	RTP cells	Human	210
hsa-miR-103a	MIMAT0000101	microRNA	33174524	2020	MicroRNA-103a Curtails the Stemness of Non-Small Cell Lung Cancer Cells by Binding OTUB1 via the Hippo Signaling Pathway	non-small cell lung cancer (NSCLC)	In NSCLC tissues and cells, miR-103a was expressed at low levels. When miR-103a was overexpressed, cell viability and stemness decreased, whereas apoptosis and cell cycle arrest were facilitated. OTUB1 expression and YAP phosphorylation decreased in the presence of miR-103a, and OTUB1 overexpression blocked the inhibitory effects of miR-103a on NSCLC cells.	Downregulation	A549	Human	211
hsa-miR-105	MIMAT0000102	microRNA	29258605	2017	miR-105 or 93-3p promotes chemoresistance and circulating miR-105 or 93-3p acts as a diagnostic biomarker for triple negative breast cancer	triple negative breast cancer (TNBC)	Therefore, a mammosphere formation assay was used to investigate the effect of miR-105 and miR-93-3p on cancer stemness. Knockdown of miR-105 or 93-3p together significantly reduced sphere size and numbers in BT-549 cells, suggesting that elevated expression of miR-105 or 93-3p may enhance chemoresistance and metastasis in TNBC patients. MiR-105 or 93-3p activates Wnt or beta-catenin signaling by downregulating SFRP1 and thereby promotes stemness, chemoresistance, and metastasis in TNBC cells.	Upregulation	BT-549, HCC70	Human	212
hsa-miR-106a	MIMAT0000103	microRNA	30011263	2018	miR-106a Reduces 5-Fluorouracil (5-FU) Sensitivity of Colorectal Cancer by Targeting Dual-Specificity Phosphatases 2 (DUSP2)	colorectal carcinoma (CRC)	DUSP2 inversely controlled the expression of COX2 to modulate stemness of cancer cells. Compared with cells transfected with miR-NC mimics, transfection of miR-106a mimics elevated expression of COX-2 and key regulators of stemness, SOX2 and OCT4. Similarly, in SW620 cells, enhanced expression of miR-106a repressed DUSP2 expression and reduced COX-2, SOX2, and OCT4 protein levels. DUSP2 was recently discovered to drive stemness of CRC cells and played a pivotal role in chemotherapy resistance. Overexpression of miR-106a significantly decreased DUSP2 mRNA and protein expression levels.MiR-106a expression is associated with stemness in CRC cells via regulation of DUSP2.	Upregulation	HCT116, SW620	Human	213
hsa-miR-106a-5p	MIMAT0000103	microRNA	33173989	2020	lncRNA TPTEP1 inhibits stemness and radioresistance of glioma through miR-106a-5p-mediated P38 MAPK signaling	glioma	TPTEP1 attenuated stemness and radioresistance of glioma both in vitro and in vivo.TPTEP1 augmented MAPK14 expression by competitively interacting with microRNA (miR)-106a-5p, thus activating the P38 MAPK signaling pathway, and suppressing glioma stemness and radioresistance. Low TPTEP2 expression levels were detected in high-grade glioma tissues compared with low-grade glioma tissues.	Upregulation	SHG44, U-251MG	Human	214
hsa-miR-107	MIMAT0000104	microRNA	31273221	2019	miR-103 or 107 prolong Wnt or beta-catenin signaling and colorectal cancer stemness by targeting Axin3	colorectal carcinoma (CRC)	Again, miR-103 or 107 overexpression led to a significant increase in the formation of secondary spheres. MiR-103 or 107 stimulate multiple stem-like features in colorectal cancer, including expression of stem-like markers, appearance of side-population cells, and capabilities in self-renewal, tumor initiation, recurrence, and chemoresistance. MiR-103 or 107 in promoting colorectal cancer stemness by targeting Axin2.	Upregulation	HCT116	Human	217
mmu-miR-146a	MIMAT0000158	microRNA	30980673	2019	RAB27B-activated secretion of stem-like tumor exosomes delivers the biomarker microRNA-146a-5p, which promotes tumorigenesis and associates with an immunosuppressive tumor microenvironment in colorectal cancer	colorectal carcinoma (CRC)	Inhibiting exosomal miR-146a with the antagomiR also impaired the spheroid formation capacity and tumorigenicity promoted by SDCSC-derived exosomes. MiRNA-146a-5p is the major miRNA in CRCSC exosomes and exosomal miR-146a promotes stem-like properties and tumorigenicity by targeting Numb in recipient CRC cells.	Upregulation	CT26	Mouse	287
mmu-miR-155	MIMAT0000165	microRNA	34689803	2021	Mechanism of exosomal miR-155 derived from bone marrow mesenchymal stem cells on stemness maintenance and drug resistance in myeloma cells	multiple myeloma	After miR-155-mimics transfection, the expression levels of proteins related to stemness maintenance marker, Hedgehog signaling, and drug resistance were increased in MPC-11 cells. BMSC-derived exosomes carrying miR-155 inhibited apoptosis, promoted cell division, and upregulated the expression of protein associated with stemness maintenance, Hedgehog signaling, and drug resistance.	Upregulation	MPC-11	Mouse	305
hsa-miR-192-5p	MIMAT0000222	microRNA	33256802	2020	Loss of miR-192-5p initiates a hyperglycolysis and stemness positive feedback in hepatocellular carcinoma	hepatocellular carcinoma (HCC)	As expected, HLF-192KO cells displayed significantly increased CSC features, such as increased populations of CD44+, CD24+ and EpCAM+ CSCs, increased mRNA levels of multiple CSC biomarkers and reduced expression of a differentiation-related gene CYP1A2, and enlarged and more spheroid formation. In CSC-positive HCCs, miR-192-5p loss enhanced glycolysis and over produced lactate might further increase HCC malignant features via interacting with environmental non-tumor cells.	Downregulation	HLF, HLE	Human	322
hsa-miR-196a	MIMAT0000226	microRNA	31352088	2019	Downregulation of microRNA-196a inhibits stem cell self-renewal ability and stemness in non-small-cell lung cancer through upregulating GPX3 expression	non-small cell lung cancer (NSCLC)	Highly-expressed miR-196a and lowly-expressed GPX3 were determined in NSCLC tissues and cells. Downregulation of miR-196a and restoration of GPX3 inhibited CSC viability, proliferation, self-renewal ability, stemness and tumorigenicity. MiR-196a promotes the development of NSCLC via activation of the JNK pathway through down-regulation of GPX3.	Upregulation	A549	Human	326
hsa-miR-199a	MIMAT0000231	microRNA	22498306	2012	MicroRNA-199a targets CD44 to suppress the tumorigenicity and multidrug resistance of ovarian cancer-initiating cells	ovarian cancer (OC)	MiR-199a significantly affected cell cycle regulation and suppressed the proliferation and invasive capacity of ovarian CICs in vitro. MiR-199a suppresses multidrug resistance and attenuates stemness in CD44+ or CD117+ ovarian CICs. MiR-199a significantly increased the chemosensitivity of ovarian CICs to cisplatin, pacitaxel, and adriamycin, and reduced mRNA expression of the multidrug resistance gene ABCG2 as compared with miR-199a mutant-transfected and untransfected cells. The expression of stemness markers was also significantly reduced in miR-199a-transfected CICs as compared with miR-199a mutant-transfected and untransfected ovarian cells.	Downregulation	ovarian cancer cancer-initiating cells (ovarian CICs)	Human	328
hsa-miR-199a-5p	MIMAT0000231	microRNA	31809227	2020	MiR-199a-5p represses the stemness of cutaneous squamous cell carcinoma stem cells by targeting Sirt1 and CD44ICD cleavage signaling	cutaneous squamous cell carcinoma (CSCC)	MiR-199a-5p is under-expressed in cSCCSCs and functions as a tumor suppressive molecule. Overexpression of miR-199a-5p reduced the stemness of cSCCSCs and inhibited cell proliferation. Overexpression of CD44ICD reversed the effects of miR-199a-5p overexpression or Sirt1 silencing, and increased the transcriptional expression of stemness genes.	Downregulation	A431	Human	331
hsa-miR-199a-3p	MIMAT0000232	microRNA	35676254	2022	Ascitic fluid shear stress in concert with hepatocyte growth factor drive stemness and chemoresistance of ovarian cancer cells via the c-Met-PI3K or Akt-miR-199a-3p signaling pathway	ovarian cancer (OC)	We observed that under conditions of shear stress or HGF treatment, where miR-199a-3p is downregulated, ovarian cancer cells were able to form more spheroids under stem cell-selective conditions. MiR-199a-3p expression is inversely related to chemoresistance of ovarian cancer and a poor clinical outcome.	Downregulation	SKOV-3, A2780	Human	329
hsa-miR-199a-3p	MIMAT0000232	microRNA	27447749	2016	miR-199a-3p targets stemness-related and mitogenic signaling pathways to suppress the expansion and tumorigenic capabilities of prostate cancer stem cells	prostate cancer (PCa)	MiR-199a-3p overexpression also diminished tumor-initiating capacities of CD44+ PCa cells as well as tumor regeneration from bulk PCa cells. Notably, miR-199a-3p inhibited secondary sphere formation in PC3 cells. Importantly, inducible miR-199a-3p expression in pre-established prostate tumors in NOD or SCID mice inhibited tumor growth.	Downregulation	DU145, PC3	Human	330
mmu-miR-205	MIMAT0000238	microRNA	26586569	2016	Downregulation of COMMD1 by miR-205 promotes a positive feedback loop for amplifying inflammatory- and stemness-associated properties of cancer cells	head and neck squamous-cell carcinoma (HNSCC)	Increased expression of miR-205 and downregulation of COMMD1 was observed in spheres derived from SAS, H460, and D121 cells. Results indicated that knockdown of COMMD1 and overexpression of miR-205 increased the expression of stemness-associated genes and sphere formation. COMMD1 downregulation by miR-205 promotes tumor development by modulating a positive feedback loop that amplifies inflammatory- and stemness-associated properties of cancer cells.	Upregulation	SAS, H460, D121	Mouse	361
hsa-miR-129-5p	MIMAT0000242	microRNA	28619508	2017	MiR-129-5p inhibits non-small cell lung cancer cell stemness and chemoresistance through targeting DLK1	non-small cell lung cancer (NSCLC)	CD133 + stem cells in both lines showed reduced miR-129-5p expression, and introducing miR-129-5p into these cells reduced stem cell markers and self-renewal ability, as measured by qRT-PCR, western blot, MTT assays, and sphere formation assays. MiR-129-5p inhibits NSCLC stemness and chemoresistance through direct targeting of DLK1.	Downregulation	A549, H460	Human	245
hsa-miR-129-5p	MIMAT0000242	microRNA	30442366	2018	LncRNA DLX6-AS1 or miR-129-5p or DLK1 axis aggravates stemness of osteosarcoma through Wnt signaling	osteosarcoma (OS)	We observed that miR-129-5p knockdown enhanced cells stemness and Wnt signaling activity, and silence of DLX6-AS1 or DLK1 in miR-129-5p-depleted MG63 and U2OS cells suppressed cells stemness and Wnt signaling activity, suggesting that the inhibitory effect of miR-129-5p on cells stemness and Wnt signaling activity could be attenuated by DLX6-AS1 or DLK1. DLX6-AS1 competitively interacted with miR-129-5p to DLK1, resulting in activation of Wnt signaling and promotion of stemness in osteosarcoma. DLX6-AS1 functionally interplayed with miR-129-6p to form a reciprocal feedback loop to activate Wnt signaling.	Downregulation	MG63, U3OS	Human	246
hsa-miR-148a	MIMAT0000243	microRNA	30551544	2019	MiR-148a suppressed cell invasion and migration via targeting WNT10b and modulating beta-catenin signaling in cisplatin-resistant colorectal cancer cells	colorectal carcinoma (CRC)	We identified the down-regulation of miR-148a in cisplatin-resistant SW480 cells. MiR-148a suppressed expression of stem cell markers, inhibited sphere formation, invasion and migration, induced apoptosis, and reduced chemo-resistance in cisplatin-resistant SW480 cells via regulating WNT10b and beta-catenin signaling pathway.	Downregulation	SW480	Human	291
hsa-miR-148a	MIMAT0000243	microRNA	26111756	2015	Bufalin Inhibits the Differentiation and Proliferation of Cancer Stem Cells Derived from Primary Osteosarcoma Cells through Mir-148a	osteosarcoma (OS)	We found that overexpression of miR-148a inhibited the self-renewing ability, the migration and invasion abilities of C1OS-CSCs. Overexpression of miR148a also inhibited the sphere formation of C1OS-CSCs. Moreover, the level of the stem cell marker Sox-2 was also down-regulated by ectopically expression of miR-148a.	Downregulation	hMG63, C1OS	Human	292
hsa-miR-148a-3p	MIMAT0000243	microRNA	32307830	2020	LncRNA HOTTIP facilitates the stemness of breast cancer via regulation of miR-148a-3p or WNT1 pathway	breast cancer (BRCA)	In this study, we found that MCF7 and T47D sphere cells had lower miR-148a-3p expression than the parental cells. In MCF7 and T47D cells, sphere formation capacity was significantly decreased in the miR-148a-3p mimic group than in the control group. We found that the inhibitory effects of depletion of HOTTIP on the self-renewal capacity of MCF7 and T47D sphere cells were reversed by the miR-148a-3p inhibitor in sphere formation assays.	Downregulation	MCF7, T47D	Human	293
hsa-miR-148a-3p	MIMAT0000243	microRNA	32268151	2020	Casticin inhibits stemness of hepatocellular carcinoma cells via disrupting the reciprocal negative regulation between DNMT1 and miR-148a-3p	hepatocellular carcinoma (HCC)	MiR-148a-3p overexpression enhanced the reduction of CAS on stemness characteristics. MiR-148a-3p also reduced mRNA level of stemness biomarkers (EpCAM, Bmi1,Nanog, and Oct4) as well as attenuated sphere formation capabilities in HCC cells. CAS could inhibit stemness characteristics in HCC cells by interruption of the reciprocal negative regulation between DNMT1 and miR-148a-3p.	Downregulation	MHCC97H, SK-Hep-1	Human	294
hsa-miR-148a-3p	MIMAT0000243	microRNA	33026174	2020	MicroRNA-148a-3p suppresses epithelial-to-mesenchymal transition and stemness properties via Wnt1-mediated Wnt or beta-catenin pathway in pancreatic cancer	pancreatic cancer (PaCa)	MiR-148a-3p expression was remarkably down-regulated in PC tissues and cell lines. In addition, functional assays demonstrated that miR-148a-3p overexpression suppressed the sphere formation ability, while miR-148a-3p depletion improved the sphere formation ability of Capan-2 cells. MiR-148a-3p suppresses PC cell proliferation, invasion, EMT and stemness properties via inhibiting Wnt1-mediated Wnt or beta-catenin pathway.	Downregulation	Capan-2	Human	295
hsa-miR-30c	MIMAT0000244	microRNA	30301667	2018	miR-30 Family Reduction Maintains Self-Renewal and Promotes Tumorigenesis in NSCLC-Initiating Cells by Targeting Oncogene TM4SF1	non-small cell lung cancer (NSCLC)	Moreover, our results showed that the gene expression level of the miR-30 family was gradually and significantly decreased during the formation of tumor spheres from SPC-A1 and NCI-H1650 cells. TM4SF1 is a direct target of miR-30a or c and miR-30a or c inhibits the stemness and proliferation of NSCLC cells by targeting TM4SF1.	Downregulation	SPC-A1, NCI-H1650	Human	422
hsa-miR-139	MIMAT0000250	microRNA	34512162	2021	miR-139 or PDE2A-Notch1 feedback circuit represses stemness of gliomas by inhibiting Wnt or beta-catenin signaling	glioblastoma (GBM)	PDE2A or miR-139 overexpression suppressed the stemness of PD-GSCs. The in vitro experiments suggested that overexpression of PDE2A and miR-139 obviously attenuated the GSC sphere formation ability. Inhibiting PDE2A by shRNA and blocking miR-139 by ASO both increased the numbers of GSC spheres. FZD3 and beta-catenin, which induced Wnt or beta-catenin signaling activation, were identified as targets of miR-139 and mediated the effects of miR-139 on GSCs. Targeted overexpression miR-139 or PDE2A in glioma with OCP system significantly repressed the stemness and decelerated glioma progression.	Downregulation	glioma cells	Human	261
hsa-miR-139-5p	MIMAT0000250	microRNA	31120140	2019	miR-139-5p reverses stemness maintenance and metastasis of colon cancer (CC) stem-like cells by targeting E2-2	colon cancer (CC)	Soft agar cloning experiments and in vitro tumorsphere formation assays demonstrated that overexpression of E2-2 in CD133+ or CD44+ HCT116 cells impaired the inhibitory effect of miR-139-5p on the self-renewal of colon cancer (CC) stem cell. MiR-139-5p targets the Wnt or beta-catenin or TCF7L2 downstream effector E2-2 in CCSCs. E2-2 is a pivot molecule in the negative feedback loop of miR-139-5p or Wnt or beta-catenin or TCF7L2. Its small interfering RNA reverses the stemness maintenance and epithelial-mesenchymal transition of colon cancer (CC) CSCs.	Downregulation	HCT116, HT-29	Human	262
hsa-miR-7	MIMAT0000252	microRNA	33837664	2021	CDR1as regulated by hnRNPM maintains stemness of periodontal ligament stem cells via miR-7 or KLF4	periodontal ligament (PDL)	CDR1as promotes the expression of stemness-related genes in PDLSCs by inhibiting miR-7-mediated suppression of KLF4 expression. Knockdown of CDR1as impairs PDLSC stemness. CDR1as maintains stemness of PDLSCs through direct interaction with miR-7, up-regulating KLF4 expression.	Downregulation	293T	Human	553
hsa-miR-7	MIMAT0000252	microRNA	26172296	2015	MicroRNA-7 inhibits the stemness of prostate cancer stem-like cells and tumorigenesis by repressing KLF4 or PI3K or Akt or p21 pathway	prostate cancer (PCa)	MicroRNA-7 is down-regulated in prostate cancer cells compared to non-tumorigenic prostate epithelial cells. Restoration of miR-7 suppresses the expression of the stemness factor KLF4 in PCSCs and inhibits prostate tumorigenesis both in vitro and in vivo. We further found that the proportion of PC3-miR-7-S-S derived large spheres was significantly decreased, which indicated a continuous inhibition of sphere formation in vitro. We found that miR-7 maintained its capability to impair the sphere formation in vitro and tumorigenesis in vivo.	Downregulation	PC3	Human	554
hsa-miR-7-5p	MIMAT0000252	microRNA	30586549	2019	MiR-7-5p suppresses stemness and enhances temozolomide sensitivity of drug-resistant glioblastoma cells by targeting Yin Yang 1	glioblastoma (GBM)	MiR-7-5p is significantly downregulated in TMZ resistant LN229 cells (LN229 or TMZ-R) compared to control cells (LN229), and low miR-7-5p expression was correlated with recurrence in GBM patients. Ectopic overexpression of miR-7-5p sensitized LN229 or TMZ-R cells to TMZ and suppressed the stemness of glioblastoma stem cells (GSCs).	Downregulation	LN229	Human	560
hsa-miR-7-5p	MIMAT0000252	microRNA	31510100	2019	Differentially Expressed microRNAs in MIA PaCa-2 and PANC-1 Pancreas Ductal Adenocarcinoma Cell Lines are Involved in Cancer Stem Cell Regulation	pancreatic ductal adenocarcinoma (PDAC)	We report the miRNA expression characteristics of two cell lines, MIA PaCa-2 and PANC-1, and discovered three miRNAs (miR-7-5p, let-7d, and miR-135b-5p) that are involved in cancer stem cells (CSCs) suppression. After transfection of each miRNA's mimic into PANC-1 cells which exhibits higher stemness feature than MIA-PaCa-2 cells, partial reduction of CSC surface markers and inhibition of tumor sphere formation were observed.	Downregulation	MIA PaCa-2,PANC-1	Human	561
hsa-miR-10a	MIMAT0000253	microRNA	32542845	2020	MicroRNA-10a promotes epithelial-to-mesenchymal transition and stemness maintenance of pancreatic cancer stem cells via upregulating the Hippo signaling pathway through WWC2 inhibition	pancreatic cancer (PaCa)	MiR-10a was highly expressed while WWC2 was lowly expressed in PC tissues. The self-renewal assay demonstrated that the number and volume of tumor microspheres were notably decreased following miR-10a inhibition, while miR-10a over-expression reversed these changes. MiR-10a inhibition reduced EMT and stemness maintenance of PCSCs via upregulating WWC2 expression and inhibiting the Hippo signaling pathway.	Upregulation	AsPC-1, BxPC-3, KP-3, PANC-1, MiaPaCa-2, HPDE6-C7	Human	218
hsa-miR-10a-5p	MIMAT0000253	microRNA	34533029	2021	microRNA-10a-5p overexpression suppresses malignancy of colon cancer (CC) by regulating human liver cancer fibroblasts	colon cancer (CC)	LX-2-miR-10a-5p CM suppresses SW480 cells migration, invasion, and spheroid formation. MiR-10a-5p overexpression inhibited the proliferation, migration, and IL-6 or IL-8 level of LX-2 cells and human liver cancer fibroblasts (HLCFs). Moreover, miR-10a-5p had lower expression in HLCFs than in human liver normal fibroblasts (HLNFs).	Downregulation	SW480	Human	219
hsa-miR-10b	MIMAT0000254	microRNA	27113763	2016	miR-10b expression in breast cancer stem cells supports self-renewal through negative PTEN regulation and sustained AKT activation	breast cancer (BRCA)	This anti-miR induced a significant decrease in miR-10b expression and a concomitant loss of the mammosphere-forming ability of enriched CSCs. Similarly, miR-10b inhibition decreased the number of mammospheres in sorted EpCAM+ MDA-MB-231 cells. Stable overexpression of miR-10b in MCF-7 cells (miR-10b-OE cells) promoted higher self-renewal and expression of stemness and epithelial-mesenchymal transition (EMT) markers.	Upregulation	MCF-7, MDA-MB-231	Human	220
hsa-miR-34a	MIMAT0000255	microRNA	33673143	2021	miR-34a and miR-200c Have an Additive Tumor-Suppressive Effect on Breast Cancer Cells and Patient Prognosis	breast cancer (BRCA)	MiR-34a and miR-200c levels are reduced in breast tumors compared to adjacent normal tissues and that this additively predicts poor patient survival. MiR-34a and miR-200c additively induce apoptosis and cell cycle arrest, while also inhibiting proliferation, invasion, migration, stemness and epithelial-to-mesenchymal transition (EMT).	Downregulation	MDA-MB-231, MCF-7	Human	441
hsa-miR-34a	MIMAT0000255	microRNA	25368020	2014	Targeting of miR34a-NOTCH1 axis reduced breast cancer stemness and chemoresistance	breast cancer (BRCA)	Our results confirm that miR34a expression was downregulated in MCF7 or ADR cells compared with MCF7 cells. Ectopic miR34a expression reduced cancer stem cell properties and increased sensitivity to doxorubicin treatment by directly targeting NOTCH1. The control mammospheres were larger and grew more rapidly than those generated following miR34a restoration. Furthermore, silencing NOTCH1 using siRNA also reduced mammosphere formation.	Downregulation	MCF7, MCF7 or ADR	Human	442
hsa-miR-34a	MIMAT0000255	microRNA	27259808	2016	Indolo-pyrido-isoquinolin based alkaloid inhibits growth, invasion and migration of breast cancer cells via activation of p53-miR34a axis	breast cancer (BRCA)	P18 significantly decreased growth, invasion and mammosphere formation in breast cancer cells which was further inhibited in the presence of miR-34a mimic. P18 increases miR-34a expression in p53-dependent manner and miR-34a is integral for P18-mediated inhibition of growth, invasion and mammosphere-formation.	Downregulation	MCF7, HBL100	Human	443
hsa-miR-34a	MIMAT0000255	microRNA	25826085	2015	Dysregulation of the miR-34a-SIRT1 axis inhibits breast cancer stemness	breast cancer (BRCA)	We found low levels of miR-34a and high levels of SIRT1 in CD44+ or CD24- breast cancer stem cells (BCSCs). MiR-34a overexpression and knockdown of SIRT1 decreased proportion of BSCSs and mammosphere formation. Expression of CSC markers, ALDH1, BMI1 and Nanog was decreased.	Downregulation	MCF-7	Human	444
hsa-miR-34a	MIMAT0000255	microRNA	25783790	2015	MicroRNA-34a suppresses the breast cancer stem cell-like characteristics by downregulating Notch1 pathway	breast cancer (BRCA)	We reported that miR-34a negatively regulated cell proliferation, migration, and invasion and breast cancer stem cell propagation by downregulating Notch1. The expression of miR-34a was negatively correlated with tumor stages, metastasis, and Notch1 expression in breast cancer tissues. Overexpression of miR-34a increased chemosensitivity of breast cancer cells to paclitaxel (PTX) by downregulating the Notch1 pathway. Mammosphere formation and expression of the stemness factor ALDH1 were also reduced in the cells treated with miR-34a and PTX compared to those treated with PTX alone.	Downregulation	MCF-7	Human	445
hsa-miR-34a	MIMAT0000255	microRNA	26359358	2015	Honokiol activates LKB1-miR-34a axis and antagonizes the oncogenic actions of leptin in breast cancer	breast cancer (BRCA)	MiR-34a mimic potentiates HNK-mediated inhibition of EMT, Zeb1 expression and nuclear-localization, mammosphere-formation, and expression of stemness factors.	Downregulation	MCF7, MDA-MB-468, MDA-MB-231	Human	446
hsa-miR-34a	MIMAT0000255	microRNA	26895471	2016	A novel miR-34a target, protein kinase D1, stimulates cancer stemness and drug resistance through GSK3 or beta-catenin signaling in breast cancer	breast cancer (BRCA)	We also found that reduction of PRKD1 by ectopic miR-34a expression or PRKD1 siRNA treatment resulted in suppressed self-renewal ability in breast cancer stem cells. Tumors from nude mice treated with miR-34a or CRT0066101 showed suppressed tumor growth, proliferation, and induced apoptosis.	Downregulation	MCF-7, MCF-7-ADR	Human	448
hsa-miR-34a	MIMAT0000255	microRNA	30005681	2018	Regorafenib suppresses colon tumorigenesis and the generation of drug resistant cancer stem-like cells via modulation of miR-34a associated signaling	colon cancer (CC)	More importantly, the addition of miR-34a mimic molecule was associated with the significantly decreased number of tumor spheres generated in both HCT-116R and DLD-1R cells. The increased miR-34a level is associated with the decreased sphere-forming ability. Western blot analysis of tumor spheres of both HCT-116R and DLD-1R treated with miR-34a mimic and inhibitor molecules. Regorafenib treatment was associated with the increased level of miR-34a, resulting in reversing drug resistance and cancer-initiating cell phenotypes by degrading WNT or beta-catenin in CRC.	Downregulation	HCT-116R, DLD-1R	Human	449
hsa-miR-34a	MIMAT0000255	microRNA	36147476	2022	Csf1r mediates enhancement of intestinal tumorigenesis caused by inactivation of Mir34a	colorectal carcinoma (CRC)	MiR-185-5p could interact with ASB16-AS1 and inhibited the progression of CRC cells. Indeed, tumoroids derived from Mir34a-deficient adenomas displayed an increase in formation rate and mean size, whereas tumoroids derived from Csf1r-deficient adenomas formed at a decreased rate and were smaller. TEAD1 (TEA domain transcription factor1) - a major effector of the Hippo signaling was proved to serve as the target of miR-185-5p and promote CRC development.	Downregulation	Lgr5-positive cells, Olfm4-positive cells	Human	450
hsa-miR-34a	MIMAT0000255	microRNA	27644439	2016	Bmi-1 regulates stem cell-like properties of gastric cancer cells via modulating miRNAs	gastric cancer (GC)	Upregulation of miR-34a may suppress the formation rate of the microspheres of gastric cancer cells, resistance to chemotherapy and cell migration, while downregulation of miR-34a can improve the formation of microspheres, chemotherapy resistance, and cell migration. Bmi-1 positively regulates stem cell-like properties via upregulating miR-21, and miR-34a negatively regulates stem cell-like characteristics by negative feedback regulation of Bmi-1 in gastric cancer.	Downregulation	MKN45	Human	451
hsa-miR-34a	MIMAT0000255	microRNA	32610494	2020	Soy Isoflavone Genistein Impedes Cancer Stemness and Mesenchymal Transition in Head and Neck Cancer through Activating miR-34a or RTCB Axis	head and neck cancer (HNC)	Genistein-induced miR-34a contributed to the ROS-associated apoptosis and diminished stemness properties via repression of RTCB in HNC-TICs.	Downregulation	S-G	Human	452
hsa-miR-34a	MIMAT0000255	microRNA	32329692	2020	Isovitexin Inhibits Stemness and Induces Apoptosis in Hepatocellular Carcinoma SK-Hep-1 Spheroids by Upregulating miR-34a Expression	hepatocellular carcinoma (HCC)	MiR-34a knockdown can reduce apoptosis and enhance the stemness of SK-Hep-1 cells. The sphere and colony formation rates, CD44+ cell population and ALDH1, ABCG2, and NANOG mRNA levels were significantly increased in SK-Hep-1 cells following transfection with anti-34a. We finally treated SK-Hep-1 cells with ISOV, anti-34a or both. We found that anti-34a antagonized the inhibitory effects of ISOV on sphere and colony formation, CD44+ population and ALDH1, ABCG2, and NANOG mRNA expression levels.	Downregulation	SK-Hep-1	Human	453
hsa-miR-34a	MIMAT0000255	microRNA	31891569	2019	Multiple Copies in T-Cell Malignancy 1 (MCT-1) Promotes the Stemness of Non-Small Cell Lung Cancer Cells via Activating Interleukin-6 (IL-6) Signaling through Suppressing MiR-34a Expression	non-small cell lung cancer (NSCLC)	MCT-1 knockdown increased the level of miR-34a, which attenuated the stemness of NSCLC cells through targeting IL-6 receptor expression. MCT-1 or miR-34a or IL-6 or IL-6R axis is responsible for MCT-1-mediated effects on NSCLC cell stemness.	Downregulation	A549	Human	454
hsa-miR-34a	MIMAT0000255	microRNA	27596137	2016	MiR-137 and miR-34a directly target Snail and inhibit EMT, invasion and sphere-forming ability of ovarian cancer cells	ovarian cancer (OC)	MiR-137 and miR-35a act as Snail suppressors to negatively regulate EMT, invasive and sphere-forming properties of OC cells.	Downregulation	SKOV-3, ES-2, NOEC	Human	455
hsa-miR-34a	MIMAT0000255	microRNA	34860809	2021	MicroRNA-34a Alleviates Gemcitabine Resistance in Pancreatic Cancer by Repression of Cancer Stem Cell Renewal	pancreatic cancer (PaCa)	MicroRNA-34a enhanced gemcitabine sensitivity both in vivo and in vitro. MicroRNA-34a suppressed the stemness and proliferation of pancreatic cancer stem cells. MicroRNA-34a directly associated with Notch 1, which lies upstream of epithelial-mesenchymal transition signaling pathways.	Downregulation	PANC-1, CFPAC-1, AsPC-1	Human	456
hsa-miR-34a	MIMAT0000255	microRNA	29187903	2017	miR34a or GOLPH3 Axis abrogates Urothelial Bladder Cancer Chemoresistance via Reduced Cancer Stemness	urothelial bladder cancer (UBC)	RT-PCR and western blotting confirmed that the expression levels of miR34a were decreased. The ectopic expression of miR34a decreased the stem cell properties of chemoresistant UBC cells and re-sensitized these cells to GC treatment in vitro and in vivo.	Downregulation	T24, 5637	Human	457
hsa-miR-34a-5p	MIMAT0000255	microRNA	36445955	2023	The miR-34a-5p-c-MYC-CHK1 or CHK2 Axis Counteracts Cancer Stem Cell-Like Properties and Enhances Radiosensitivity in Hepatocellular Cancer Through Repression of the DNA Damage Response	hepatocellular carcinoma (HCC)	We observed that miR-34a-5p downregulated LM3 cells formed spheres that were significantly greater in number and larger in size than negative control-transfected LM3 cells. The miR-34a-5p-c-MYC-CHK1 or CHK2 axis counteracts cancer stem cell-like properties and enhances radiosensitivity in hepatocellular cancer through repression of the DNA damage response.	Downregulation	SMMC-7721, Huh7, LM3	Human	458
hsa-miR-181a	MIMAT0000256	microRNA	35029026	2022	Autophagy inhibits cancer stemness in triple-negative breast cancer via miR-181a-mediated regulation of ATG5 and or or ATG2B	breast cancer (BRCA)	MiR-181a expression is upregulated in both TNBC CSCs and patient tissues. In addition, tumorsphere formation ability of TNBC cells transfected with the miR-181a inhibitor was found to be impaired. Inhibition of miR-181a expression led to attenuation of TNBC stemness and an increase in autophagy flux.	Upregulation	MDA-MB-231, MDA-MB-231, MCF7	Human	313
hsa-miR-181a	MIMAT0000256	microRNA	28389242	2017	Upregulation of miR-181a suppresses the formation of glioblastoma stem cells by targeting the Notch2 oncogene and correlates with good prognosis in patients with glioblastoma multiforme	glioblastoma (GBM)	MiR-181a was downregulated in GSCs derived from human glioblastoma U87MG and U373MG cells. The high expression of miR-181a inhibited the levels of stemness-related markers CD133 and BMI1, attenuated sphere proliferation, promoted cell apoptosis, and reduced the tumorigenicity of GSCs.	Downregulation	U87MG, U373MG	Human	314
hsa-miR-181a	MIMAT0000256	microRNA	33574092	2021	The miR-181a-SFRP4 Axis Regulates Wnt Activation to Drive Stemness and Platinum Resistance in Ovarian Cancer	high-grade serous ovarian cancer (HGSOC)	Using our miR-181a sensor, we dichotomized each cell line into miR-181aHigh and miR-181aLow subpopulations and confirmed that the miR-181aHigh subpopulations exhibited increased stem cell capacity using an in vitro extreme limiting dilution sphere formation assay. MiR-181a is an activator of Wnt signaling that drives stemness and chemoresistance in HGSOC.	Upregulation	HEYA8, OCI-P5X, OV81.2-CP10	Human	315
hsa-miR-181b	MIMAT0000257	microRNA	30470250	2018	miR-181b or Notch2 overcome chemoresistance by regulating cancer stem cell-like properties in NSCLC	non-small cell lung cancer (NSCLC)	Ectopic miR-181b expression suppressed cancer stem cell properties and enhanced sensitivity to cisplatin (DDP) treatment by directly targeting Notch2. A549 or DDP cells formed more and larger tumourspheres than did A549 cells. Cells with miR-181b formed fewer and smaller tumourspheres than did cells transfected with the negative control. More and larger tumourspheres formed following anti-miR-181b exposure in A549 cells.	Downregulation	A549, H1650, H1299	Human	317
hsa-miR-183	MIMAT0000261	microRNA	27431799	2016	MicroRNA-183 suppresses cancer stem-like cell properties in EBV-associated nasopharyngeal carcinoma	nasopharyngeal carcinoma (NPC)	Downregulation of miR-96 and miR-183 was confirmed in NPC spheroids. That ectopic expression of miR-96 and miR-183 suppressed cell growth and tumor sphere formation in NPC. The tumorigenicity of cells stably expressing miR-183 was significantly inhibited in the in vivo nude mice model.	Downregulation	C666-1	Human	318
hsa-miR-203	MIMAT0000264	microRNA	31544978	2020	MicroRNA-203 diminishes the stemness of human colon cancer (CC) cells by suppressing GATA6 expression	colon cancer (CC)	Overexpression and sequestration of miR-203 in HCT-116 and HT-29 human CRC cells reduces and enhances their stemness, respectively. Silencing the expression of either LRH-1 or Hes-1 is sufficient to diminish the stemness-promoting effects of GATA6 in human CRC cells.	Downregulation	HCT-116, HT-29	Human	347
hsa-miR-203	MIMAT0000264	microRNA	24145190	2014	Maintenance of the stemness in CD44+ HCT-15 and HCT-116 human colon cancer (CC) cells requires miR-203 suppression	colorectal carcinoma (CRC)	Silencing miR-203 expression in wild-type HCT-116 human colon cancer (CC) cells also resulted in an increase of their stemness. We show for the first time that the downregulation of miR-203 by HA or CD44 signaling is the main reason for stemness-maintenance in colon cancer (CC) cells.	Downregulation	HCT-15, HCT-116, HT-29	Human	348
hsa-miR-203	MIMAT0000264	microRNA	27484906	2016	MicroRNA-203 As a Stemness Inhibitor of Glioblastoma Stem Cells	glioblastoma (GBM)	MiR-296-5p inhibits GBM cell stemness and their capacity to self-renew as spheres and propagate glioma xenografts in vivo.	Downregulation	glioblastoma stem cells (GBM-SCs)	Human	349
hsa-miR-203	MIMAT0000264	microRNA	31016725	2019	MicroRNA-203 reinforces stemness properties in melanoma and augments tumorigenesis in vivo	melanoma	MiR-203 could be down-regulated in melanoma tissues but be overexpressed in melanoma stem cells. It has an important role as oncomiR and promote repopulation, tumorigenicity, self-renewal, and migration.	Upregulation	A375, NA8, D10	Human	350
hsa-miR-203	MIMAT0000264	microRNA	27589832	2016	A directly negative interaction of miR-203 and ZEB2 modulates tumor stemness and chemotherapy resistance in nasopharyngeal carcinoma	nasopharyngeal carcinoma (NPC)	MiR-203 suppressed cell migration, invasion, tumor stemness, and chemotherapy resistance to cisplatin (DDP) in vitro and in vivo. MiR-203 was negatively correlated with ZEB2 expression in NPC tissues and tumor spheres.	Downregulation	5-8F, 6-10B	Human	351
hsa-miR-203	MIMAT0000264	microRNA	29552304	2018	The PCAT3 or PCAT9-miR-203-SNAI2 axis functions as a key mediator for prostate tumor growth and progression	prostate cancer (PCa)	Knockdown of PCAT3 and PCAT9 suppressed cellular proliferation, invasion, migration, angiogenesis and stemness in androgen-dependent LNCaP and 22Rv1 cells. Silence of miR-203 or ectopic expression of SNAI2 attenuated the inhibitory effect of PCAT3 and PCAT11 knockdown on cell proliferation and migration in vitro, and xenograft growth in vivo.	Downregulation	LNCaP, 22Rv1	Human	352
hsa-miR-203	MIMAT0000264	microRNA	29389061	2018	The miR-203 or SNAI2 axis regulates prostate tumor growth, migration, angiogenesis and stemness potentially by modulating GSK-3beta or beta-CATENIN signal pathway	prostate cancer (PCa)	MiR-203 was significantly downregulated in prostate cancer cell lines compared with immortalized prostate epithelial cells. MiR-203 inhibited prostate cancer cell proliferation, migration, endothelial cell tube formation and cancer stemness in vitro. The in vivo study showed that miR-203 suppressed tumorigenicity, metastasis and angiogenesis of DU145 cells.	Downregulation	DU145, PC3	Human	353
hsa-miR-203	MIMAT0000264	microRNA	29440295	2018	MicroRNA-203 Inhibits Long Noncoding RNA HOTAIR and Regulates Tumorigenesis through Epithelial-to-mesenchymal Transition Pathway in Renal Cell Carcinoma	renal cell carcinoma (RCC)	MiR-203 was significantly underexpressed in RCC cell lines and clinical specimens compared with normal cell line and tissue. Overexpression of miR-203 significantly inhibited proliferation, migration, and invasion with an induction of apoptosis and cell-cycle arrest. MiR-203-mediated regulation of HOTAIR induces tumor suppressor effects in RCC by regulating EMT and metastatic pathway genes.	Downregulation	HK-2, ACHN, Caki-1	Human	354
hsa-miR-204	MIMAT0000265	microRNA	23204229	2013	Loss of miR-204 expression enhances glioma migration and stem cell-like phenotype	glioma	We report the results of a differential miRNA expression screen that compared glioma and neural stem cells, where we found that miR-204 was markedly downregulated in both types of cells. Restoring miR-204 expression in glioma cells suppressed tumorigenesis and invasiveness in vivo and increased overall host survival.	Downregulation	LN382T, SNB19	Human	355
hsa-miR-204	MIMAT0000265	microRNA	26933999	2016	Suppression of miR-204 enables oral squamous cell carcinomas to promote cancer stemness, EMT traits, and lymph node metastasis	oral squamous cell carcinoma (OSCC)	MiR-204 over-expression suppresses cancer stemness and in vivo tumor-growth of OSCC-CSCs. On the contrary, down-regulation of miR-204 significantly increased cancer stemness and the lymph nodes incidence of orthotopic animal models.	Downregulation	S-G, SAS, OECM-1	Human	356
hsa-miR-204-5p	MIMAT0000265	microRNA	35930907	2022	Dysregulation of miR-204-5p or APLN axis affects malignant progression and cell stemness of esophageal cancer	esophageal cancer (ESCA)	MiR-204-5p was lowly expressed while its target gene APLN was highly expressed in tumor tissues. Besides, miR-204-5p overexpression hindered proliferation, invasion, migration, and stemness of EC cells. Dysregulation of miR-204-5p or APLN axis was linked with malignant progression of EC.	Downregulation	ECa-109, TE-1	Human	357
hsa-miR-204-5p	MIMAT0000265	microRNA	31938073	2020	MicroRNA-204-5p is a tumor suppressor and potential therapeutic target in head and neck squamous cell carcinoma	head and neck squamous-cell carcinoma (HNSCC)	We reveal that miR-204-5p as a tumor suppressor is commonly repressed in HNSCC, which can inhibit tumor growth, metastasis and stemness. MiR-204-5p-SNAI2 or SUZ12 or HDAC1 or STAT3 regulatory circuit has a critical role in maintaining aggressiveness of HNSCC.	Downregulation	SCC9, SCC15, SCC25, UM1	Human	358
hsa-miR-205	MIMAT0000266	microRNA	24911147	2014	MicroRNA-205 signaling regulates mammary stem cell fate and tumorigenesis	breast cancer (BRCA)	Knockdown of miR-205 in mammary epithelial cells promoted epithelial-mesenchymal transition (EMT), disrupted epithelial cell polarity, and enhanced symmetric division to expand the stem cell population. Furthermore, miR-205-deficient mice spontaneously developed mammary lesions, while activation of miR-205 markedly diminished breast cancer stemness.	Downregulation	MCF12A, MDA-MB231, BT549	Human	359
hsa-miR-205	MIMAT0000266	microRNA	26586569	2016	Downregulation of COMMD1 by miR-205 promotes a positive feedback loop for amplifying inflammatory- and stemness-associated properties of cancer cells	head and neck squamous-cell carcinoma (HNSCC)	Increased expression of miR-205 and downregulation of COMMD1 was observed in spheres derived from SAS, H460, and D121 cells. Results indicated that knockdown of COMMD1 and overexpression of miR-205 increased the expression of stemness-associated genes and sphere formation. COMMD1 downregulation by miR-205 promotes tumor development by modulating a positive feedback loop that amplifies inflammatory- and stemness-associated properties of cancer cells.	Upregulation	SAS, H460, D121	Human	360
hsa-miR-205	MIMAT0000266	microRNA	29964204	2018	Integrin alpha5 down-regulation by miR-205 suppresses triple negative breast cancer stemness and metastasis by inhibiting the Src or Vav2 or Rac1 pathway	triple negative breast cancer (TNBC)	MiR-205 expression level is extremely low in basal mesenchymal-like highly migratory and invasive TNBC cells. Stably re-expressing miR-205 in TNBC cells significantly reduced their migration, invasion capability and cancer stem cell (CSC)-like property. ITGA5 down-regulation by miR-205 re-expression impairs TNBC cell metastatic traits by inhibiting the Src or Vav2 or Rac1 pathway.	Downregulation	SUM-159	Human	362
hsa-miR-210	MIMAT0000267	microRNA	24930954	2014	Knockdown of miR-210 decreases hypoxic glioma stem cells stemness and radioresistance	glioma	Knockdown of miR-210 decreased neurosphere formation capacity, stem cell marker expression and cell viability, and induced differentiation and G0 or G1 arrest in hypoxic GSCs by partially rescued Myc antagonist (MNT) protein expression. Moreover, knockdown of miR-210 led to increased apoptotic rate and Caspase-3 or 7 activity and decreased invasive capacity, reactive oxygen species (ROS) and lactate production and radioresistance in hypoxic GSCs.	Upregulation	U87, SHG44	Human	374
hsa-miR-211	MIMAT0000268	microRNA	33536579	2021	MiR-211 determines brain metastasis specificity through SOX11 or NGN2 axis in triple-negative breast cancer	breast cancer (BRCA)	Sphere numbers were significantly increased in high miR-211-expressing cells compared with control cells, sphere numbers were significantly increased in miR-211 overexpressing HCC1806 cells.	Upregulation	HCC1806, MDA-MB-231	Human	376
hsa-miR-214	MIMAT0000271	microRNA	26299367	2015	Targeting the Wnt-Regulatory Protein CTNNBIP1 by microRNA-214 Enhances the Stemness and Self-Renewal of Cancer Stem-Like Cells in Lung Adenocarcinomas	lung adenocarcinoma (LUAD)	MiR-214 overexpression enhances stem-like properties in LAC cells and that miR-214 shows increased expression in CSLCs derived from primary tumor tissue and from two LAC cell lines (A549 and NCI-H1650). Downregulation of miR-214 expression in CSLCs resulted in a significant decrease in spheroid formation and the expression of the stem-cell markers Nanog, Oct-4, and Sox-2.	Upregulation	A549, NCI-H1650	Human	377
hsa-miR-215	MIMAT0000272	microRNA	25775580	2015	The CDX1-microRNA-215 axis regulates colorectal cancer stem cell differentiation	colorectal carcinoma (CRC)	MiR-215 expression is depleted in FACS-enriched cancer stem cells compared with unsorted samples. The cell lines LS174T and LOVO, in addition to forming more total colonies after miR-215 knockdown, also displayed a marked shift away from their typical morphologies and toward a larger, denser, regularly spherical colony shape. Overexpression of miR-215 in poorly differentiated cell lines causes a decrease in clonogenicity. We identified the genome-wide targets of miR-215 and found that miR-215 mediates the repression of cell cycle and stemness genes downstream of CDX1. The miR-215 target gene BMI1 has been shown to promote stemness and self-renewal and to vary inversely with CDX1.	Downregulation	LS174T, LOVO	Human	378
hsa-miR-216a	MIMAT0000273	microRNA	32230799	2020	miR-216a Acts as a Negative Regulator of Breast Cancer by Modulating Stemness Properties and Tumor Microenvironment	breast cancer (BRCA)	Overexpression of miR-216a-5p impairs stemness markers, mammosphere formation, ALDH activity, and the level of Toll-like receptor 4 (TLR4), which plays a significant role in breast cancer progression and metastasis by leading to the release of pro-inflammatory molecules, such as interleukin 6 (IL-6).	Downregulation	MDA-MB-231, T47D	Human	382
hsa-miR-216a	MIMAT0000273	microRNA	29496393	2018	Morin inhibits proliferation and self-renewal of CD133+ melanoma cells by upregulating miR-216a	melanoma	Either Morin treatment or miR-216a overexpression reduced cell viability, sphere formation ability and expressions of stem cell marker genes CD20, CD44, CD133 and Wnt-3A. Inhibition of the stemness marker gene expressions in CD133+ melanoma cells is mediated by downregulating Wnt-3A through miR-216a.	Downregulation	MV3, M14	Human	383
hsa-miR-217	MIMAT0000274	microRNA	28849121	2017	miR-217 targeting DKK1 promotes cancer stem cell properties via activation of the Wnt signaling pathway in hepatocellular carcinoma	hepatocellular carcinoma (HCC)	MiR-217 expression was markedly increased in HCC tissues and cells. Overexpression of miR-217 promoted, while silencing miR-217 suppressed, the fraction of the side population and the expression of cancer stem cell factors in vitro and tumorigenicity in vivo in HCC cells.	Upregulation	HepG2, Huh7	Human	387
hsa-miR-218	MIMAT0000275	microRNA	27926533	2017	Andrographolide impedes cancer stemness and enhances radio-sensitivity in oral carcinomas via miR-218 activation	oral squamous cell carcinoma (OSCC)	Knockdown of miR-218 in ALDH1-CD44- non-OCSCs enhanced cancer stemness, while silencing of Bmi1 significantly counteracted it. We showed that silencing of endogenous miR-218 induced sphere-forming capability in non-CSCs, which was abolished by knockdown of Bmi1.	Downregulation	NHOK,ALDH+ OCSCs,CD44+ OCSCs	Human	388
hsa-miR-218	MIMAT0000275	microRNA	30008871	2018	MicroRNA-218 inhibits the migration, epithelial-mesenchymal transition and cancer stem cell properties of prostate cancer cells	prostate cancer (PCa)	MiR-218 was downregulated in 2 PCa cell lines and could suppress cell migration, EMT and the exhibition of cancer stem cell-like properties. In these experiments, the control cells generated more tumor-spheres than the miR-218-overexpressing cells in both cell lines.	Downregulation	LNCaP,C4-2	Human	389
hsa-miR-218-5p	MIMAT0000275	microRNA	32784466	2020	Targeting BC200 or miR218-5p Signaling Axis for Overcoming Temozolomide Resistance and Suppressing Glioma Stemness	glioblastoma (GBM)	Thus, we wanted to investigate the relevance of miR-218-5p in controlling the self-renewal potential and TMZ resistance of GB cells. The self-renewal and pluripotency properties of GB cells were analyzed by targeting miR-218-5p. The inhibition of miR-218-5p showed a significantly higher tumorsphere and colony-forming abilities in GB cells than in the control (NC) mock-transfected groups. Moreover, markers for self-renewal and ABC Transporters in miR-218-5p-inhibited GB cells were evaluated. Markers such as Oct4, SOX2, KLF4, BCRP1, MDR1, and MRP1 were observed to be upregulated in miR-218-5p-inhibited cells compared with control NC and mock-transfected cells.	Downregulation	U87MG, GBM8901	Human	390
hsa-miR-221	MIMAT0000278	microRNA	26556862	2016	MiR-221 promotes stemness of breast cancer cells by targeting DNMT3b	breast cancer (BRCA)	We found that miR-221 was upregulated in BCSCs compared to their differentiated counterpart. Transfection of miR-221 in T47D cells increased the number of mammospheres and the expression of stem cell markers.	Upregulation	T47D	Human	391
hsa-miR-221	MIMAT0000278	microRNA	28844858	2017	miR-221 or 222 promote cancer stem-like cell properties and tumor growth of breast cancer via targeting PTEN and sustained Akt or NF-kappaB or COX-2 activation	breast cancer (BRCA)	MiR-221 or 222 were overexpressed in highly aggressive breast cancer MDA-MB-231 cells, that are enriched in markers for epithelial-mesenchymal transition (EMT) and BCSCs, than in MCF-7 cells.MiR-221 or 222 enhanced breast cancer cell growth, migration and invasion by downregulating PTEN. Both ectopic expression of miR-221 or 222 and PTEN knockdown increased the mammosphere formation capacity and the expression of the stemness marker ALDH1.	Upregulation	MCF-7, MDA-MB-231	Human	392
hsa-miR-221	MIMAT0000278	microRNA	30110679	2018	Increased Cellular Levels of MicroRNA-9 and MicroRNA-221 Correlate with Cancer Stemness and Predict Poor Outcome in Human Breast Cancer	breast cancer (BRCA)	Knockdown of both miR-9 and miR-221 in invasive MDA-MB-232 breast cancer cells dramatically decreased the number of side-population colonies with stem cell-like potency, which reduced the capacity for tumor-cell renewal, invasion, and migration. Upon transfection of cells with both miRNA inhibitors, the number of tumorsphere-forming MDA-MB-231 cells was reduced by > 80percentage together with a reduction in the transcription of the stemness markers CD133, Nanog, and Oct4 genes.	Upregulation	MCF-7, MDA-MB-231	Human	393
hsa-miR-222	MIMAT0000279	microRNA	28844858	2017	miR-221 or 222 promote cancer stem-like cell properties and tumor growth of breast cancer via targeting PTEN and sustained Akt or NF-kappaB or COX-2 activation	breast cancer (BRCA)	MiR-221 or 222 were overexpressed in highly aggressive breast cancer MDA-MB-231 cells, that are enriched in markers for epithelial-mesenchymal transition (EMT) and BCSCs, than in MCF-7 cells.MiR-221 or 222 enhanced breast cancer cell growth, migration and invasion by downregulating PTEN. Both ectopic expression of miR-221 or 222 and PTEN knockdown increased the mammosphere formation capacity and the expression of the stemness marker ALDH2.	Upregulation	MCF-7,MDA-MB-231	Human	394
hsa-miR-222	MIMAT0000279	microRNA	26420065	2015	PBX3 is targeted by multiple miRNAs and is essential for liver tumour-initiating cells	hepatocellular carcinoma (HCC)	We used the TIC-enriched Hep-12 and the non-tumorigenic Hep-11 cell lines by genome-wide profiling of miRNA expression with miRNA microarray analysis, followed by functional screening with soft-agar assay and we got let-7c, miR-200b, miR-222 and miR-424 which resulted in a complete inhibition of tumour formation. The spheroid formation efficiency decreased significantly when the expression of the four miRNAs was induced individually by DOX.	Downregulation	Hep-12, Huh7	Human	395
hsa-miR-223-3p	MIMAT0000280	microRNA	35588441	2022	LncRNA PITPNA-AS1 or miR-223-3p or PTN axis regulates malignant progression and stemness in lung squamous cell carcinoma	lung squamous cell carcinoma (LUSC)	Repression of PITPNA-AS1 retarded tumor spheres formation, although this impact may be countered by miR-223-3p inhibitors or PTN overexpression. MiR-223-3p inhibition or PTN overexpression might reverse the inhibitory effects of PITPNA-AS1 suppression on LUSC progression, as demonstrated by rescue experiments. In addition, the PITPNA-AS1 or miR-223-3p or PTN axis accelerated tumor development in vivo.	Downregulation	SK-MES-1, NCI-H520, NCI-H226, NCI-H2170, BEAS-2B	Human	396
hsa-miR-200b	MIMAT0000318	microRNA	35951366	2022	Dicer-mediated miR-200b expression contributes to cell migratory or invasive abilities and cancer stem cells properties of breast cancer cells	breast cancer (BRCA)	Suppression of Dicer inhibited miR-200b expression, whereas miR-200b suppression recovered Dicer knockdown-induced migration, invasion, and cancer stem cells (CSCs) properties of the breast cancer cells. By contrast, the overexpression of miR-200b in the MCF-7 or shDicer cells reduced sphere diameter and quantity.	Downregulation	MCF-7	Human	336
hsa-miR-200b	MIMAT0000318	microRNA	32495507	2020	Hepatocyte nuclear factor-1beta suppresses the stemness and migration of colorectal cancer cells through promoting miR-200b activity	colorectal carcinoma (CRC)	It must be noted that the sphere size between HNF-1beta-OE and HNF-1beta-OE and miR-200b-kd was similar in SW620 cells, which means that miR-200b knockdown rescued the inhibitory effects of HNF-1beta-OE on sphere-formation ability through regulating the sphere number but not sphere size in SW620 cells. HNF-1beta suppressed the stemness and migration of colorectal cancer cells.HNF-1beta inhibits the stemness and migration of colorectal cancer cells through miR-200b.	Downregulation	SW620, HT-29	Human	337
hsa-miR-200b	MIMAT0000318	microRNA	26420065	2015	PBX3 is targeted by multiple miRNAs and is essential for liver tumour-initiating cells	hepatocellular carcinoma (HCC)	We used the TIC-enriched Hep-12 and the non-tumorigenic Hep-11 cell lines by genome-wide profiling of miRNA expression with miRNA microarray analysis, followed by functional screening with soft-agar assay and we got let-7c, miR-200b, miR-222 and miR-424 which resulted in a complete inhibition of tumour formation. The spheroid formation efficiency decreased significantly when the expression of the four miRNAs was induced individually by DOX.	Downregulation	Hep-12, Huh7	Human	338
hsa-miR-200b	MIMAT0000318	microRNA	28383782	2017	The miR-200b-ZEB1 circuit regulates diverse stemness of human hepatocellular carcinoma	hepatocellular carcinoma (HCC)	MiR-200b downregulation occurred in early HCC and associated with poor prognosis. We found that ectopic expression of miR-200b in HepG2 and Tong cells suppressed both anchorage-independent growth in soft agars and tumorspheres in 3-D culture. Notably, tumorsphere formation in 3-D culture, which represents the capacity for tumor initiation, has been used as an in vitro indicator of cancer cell stemness. Ectopic expression of miR-200b or silencing of ZEB1 led to a decrease in CD13+ and CD24+ HCC CSCs and an increase in EpCAM+ HCC CSCs. Silencing CD13 or CD24 expression suppressed tumorigenicity of HCC cells.	Downregulation	SK-Hep1, HepG2, PLC5, Huh7, Tong	Human	339
hsa-miR-15b-5p	MIMAT0000417	microRNA	32398664	2020	CircZNF609 enhances hepatocellular carcinoma cell proliferation, metastasis, and stemness by activating the Hedgehog pathway through the regulation of miR-15a-5p or 15b-5p and GLI2 expressions	hepatocellular carcinoma (HCC)	Similarly, GLI2 upregulation or miR-15a-5p or 15b-5p suppression recovered circZNF609 depletion-mediated inhibitive effect on cell sphere formation ability to different degrees. CircZNF609 enhances HCC cell proliferation, metastasis, and stemness by activating the Hedgehog pathway through the regulation of miR-15a-5p or 15b-5p and GLI2 expressions.	Upregulation	HCCLM3, MHCC-97H	Human	311
hsa-miR-23b	MIMAT0000418	microRNA	28449663	2017	MiR-23b controls ALDH1A1 expression in cervical cancer stem cells	cervical cancer (CC)	MiR-23b was under-expressed in cervical cancer stem cells to maintain high levels of ALDH1A1.Overexpression of miR-23b in Hela cells dramatically reduce the size and number of tumorspheres. Introduction of miR-23b into cervical cancer cells could alter stemness and cisplatin sensitivity.	Downregulation	Hela, CaSki, C33A, Siha	Human	398
hsa-miR-27b-3p	MIMAT0000419	microRNA	34334630	2021	LncRNA AFAP1-AS1 or miR-27b-3p or VEGF-C axis modulates stemness characteristics in cervical cancer cells	cervical cancer (CC)	We suppressed miR-27b-3p by using miR-27b-3p-inhibitor in the CD44v6+ Hela cells. The inhibitory effects of AFAP1-AS1 knockdown on cell cycle transition of G(1) or S phase, the cell stemness, and EMT-related markers in the CD44v6+cells were all recovered by miR-27b-3p suppression.	Downregulation	Hela	Human	403
hsa-miR-30b-5p	MIMAT0000420	microRNA	33760161	2021	LncRNA GATA3-AS1-miR-30b-5p-Tex10 axis modulates tumorigenesis in pancreatic cancer	pancreatic cancer (PaCa)	MiR-30b-5p downregulation and GATA3-AS1 upregulation were revealed in PC tissues and cell lines. The miR-30b-5p-Tex10 axis was confirmed to be involved in the regulation of biological effects of GATA3-AS1, including cell viability, cell proliferation, cell invasion, cell apoptosis, and cell stemness, as well as Wnt1 or beta-catenin signaling.	Downregulation	PANC-1, AsPC-1	Human	421
hsa-miR-122	MIMAT0000421	microRNA	30341415	2019	MicroRNA-122 negatively associates with peroxiredoxin-II expression in human gefitinib-resistant lung cancer stem cells	lung cancer (LC)	MiR-122 inhibited A549 or GR stemness by downregulating the Hedgehog, Notch, and Wnt or beta-catenin pathways. Furthermore, smaller spheres and fewer spheres observed in sphere-formation assays indicated the reduction of the self-renewal ability of A549 or GR CSC after miR-122 transfection.	Downregulation	A549, H460, HCC827	Human	222
hsa-miR-122-5p	MIMAT0000421	microRNA	36582605	2022	Cancer stem cell-like cells-derived exosomal lncRNA CDKN2B-AS1 promotes biological characteristics in thyroid cancer via miR-122-5p or P4HA2 axis	thyroid cancer	CDKN2B-AS1 and P4HA1 expressions were up-regulated, and miR-122-5p expression was down-regulated in thyroid cancer. sh-CDKN2B-AS1 hindered tumor sphere formation. CSCs-derived exosomal CDKN2B-AS1 acts as an oncogene in thyroid cancer through miR-122-5p or P4HA2 axis.	Downregulation	TPC-1, SW579	Human	223
hsa-miR-124	MIMAT0000422	microRNA	27765948	2016	Suppression of iASPP-dependent aggressiveness in cervical cancer through reversal of methylation silencing of microRNA-124	cervical cancer (CC)	Hela cells transfected with miR-124 mimic exhibited round and enlarged morphological changes and less motility and invasion as well as weaker proliferative and sphere-forming abilities than cells transfected with the mimic control. The expression of iASPP could relieve miR-124-mediated inhibition of invasion, proliferation and sphere formation. MiR-124, directly targeting iASPP, reduces expression of iASPP and attenuates CC cell growth and invasiveness.	Downregulation	Hela, Siha	Human	224
hsa-miR-124	MIMAT0000422	microRNA	24705396	2014	MiR-124 Radiosensitizes human colorectal cancer cells by targeting PRRX1	colorectal carcinoma (CRC)	We found that miR-124 was significantly down-regulated both in CRC-derived cell lines and clinical CRC samples compared with adjacent non-tumor colorectal tissues, MiR-124 could sensitize human colorectal cancer cells to IR in vitro and in vivo. Western blot analysis showed that PRRX1 could reverse the expression of EMT and stemness-related genes caused by overexpression of miR-124. We illustrated that miR-124 could increase the radiosensitivity of CRC cells by blocking the expression of PRRX1.	Downregulation	SW480, LOVO	Human	225
hsa-miR-124	MIMAT0000422	microRNA	32681617	2020	MicroRNA-124 inhibits stem-like properties and enhances radiosensitivity in nasopharyngeal carcinoma cells via direct repression of expression of JAMA	nasopharyngeal carcinoma (NPC)	Down-regulation of miR-124 was detected in cancer tissues and was inversely associated with tumour stage and lymph node metastasis. CSCs are abundant in non-adherent spherical cell clusters, termed tumorspheres. Tumorsphere formation assays showed that miR-124 inhibited their generation. The number of tumorspheres was 42percentage-63percentage lower, and tumours were also significantly smaller, in cells transfected with miR-124 mimic, compared with untransfected control cells. Furthermore, results from tumorsphere formation assays indicated that more and larger spheres were formed in cells with miR-124 down-regulated than in controls. Overexpression of miR-124 inhibited stemness properties and enhanced radiosensitivity of NPC cells in vitro and in vivo via targeting JAMA.	Downregulation	CNE2, HONE1	Human	226
hsa-miR-124a	MIMAT0000422	microRNA	20665740	2010	miR-124a is important for migratory cell fate transition during gastrulation of human embryonic stem cells	gastrulation	MiR-124a may play an active role in inhibiting hESCs from differentiation into EB by downregulating expression of SLUG and IQGAP1, thereby maintaining stemness.	Downregulation	H9	Human	232
hsa-miR-124a	MIMAT0000422	microRNA	29702194	2018	Tumor suppressive microRNA-124a inhibits stemness and enhances gefitinib sensitivity of non-small cell lung cancer cells by targeting ubiquitin-specific protease 14	non-small cell lung cancer (NSCLC)	Hsa-miR-124a was downregulated during spheroid formation of the NSCLC cell lines SPC-A1 and NCI-H1650 and NSCLC tissues compared with normal lung cells and tissues. USP14 is a direct target of hsa-miR-124a, and that hsa-miR-124a inhibits stemness and enhances the gefitinib sensitivity of NSCLC cells by targeting USP14.	Downregulation	SPC-A1, NCI-H1650	Human	233
hsa-miR-125b	MIMAT0000423	microRNA	25953743	2015	MicroRNA-125b attenuates epithelial-mesenchymal transitions and targets stem-like liver cancer cells through small mothers against decapentaplegic 2 and 4	hepatocellular carcinoma (HCC)	We found down-regulation of miR-125b in most HCC cells and clinical specimens. Moreover, miR-125b overexpression reduced the tumor sphere diameter compared with control-transfected cells (28.13 percentage and 33.37 percentage decrease in Huh751 cells and Li-7 cells). We found that miR-125b attenuated EMT-associated traits, including chemoresistance, migration, and stemness in HCC cells, and negatively correlated with EMT and cancer stem cell (CSC) marker expressions in HCC specimens.	Downregulation	Huh751, Li-7	Human	236
hsa-miR-128-3p	MIMAT0000424	microRNA	28627514	2017	Simultaneous overactivation of Wnt or beta-catenin and TGFbeta signalling by miR-128-3p confers chemoresistance-associated metastasis in NSCLC	non-small cell lung cancer (NSCLC)	Furthermore, miR-128-3p was upregulated in tumour sphere-derived NSCLC cells, compared with their parental cells. In parallel, miR-128-3p overexpression greatly potentiated the self-renewal ability of the NSCLC cells to grow into more, larger-sized non-adherent cell spheres and increased the proportions of stem cell-like SP fractions. MiR-128-3p induces mesenchymal and stemness-like properties through downregulating multiple inhibitors of Wnt or beta-catenin and TGF-beta pathways, leading to their overactivation. Importantly, antagonism of miR-128-3p potently reverses metastasis and chemoresistance of highly malignant NSCLC cells, which could be completely reversed by restoring Wnt or beta-catenin and TGF-beta activities.	Upregulation	A549, Calu-3, H520	Human	240
hsa-miR-133a-3p	MIMAT0000427	microRNA	31660998	2019	Methylation-mediated silencing of miR-133a-3p promotes breast cancer cell migration and stemness via miR-133a-3p or MAML1 or DNMT3A positive feedback loop	breast cancer (BRCA)	MiR-133a-3p was down-regulated in all three types of sphere breast cancer cells compared with the corresponding normal breast cancer cells. Reducing miR-133a-3p expression led to a significant increase in the migration, invasion, proliferation, and stemness of breast cancer cells in vitro.	Downregulation	MCF-7, MDA-MB-468, MDA-MB-231	Human	250
hsa-miR-137	MIMAT0000429	microRNA	23714687	2013	MicroRNA-137 is downregulated in glioblastoma and inhibits the stemness of glioma stem cells by targeting RTVP-1	glioblastoma (GBM)	We found that the expression of miR-137 was significantly lower in GBM and GSCs compared to normal brains and neural stem cells (NSCs). Transduction of the GSC neurospheres with lentivirus vector expressing pre-miR-137 significantly decreased the secondary neurosphere formation by 6.6-fold, 3.3-fold, and 2.8-fold, respectively, compared with GSCs that were transduced with a lentivirus vector expressing a control pre-miR. MiR-137 inhibits GSC self-renewal and promotes their differentiation by targeting RTVP-1 which downregulates CXCR4.	Downregulation	HF2355, HF2414	Human	257
hsa-miR-137	MIMAT0000429	microRNA	27596137	2016	MiR-137 and miR-34a directly target Snail and inhibit EMT, invasion and sphere-forming ability of ovarian cancer cells	ovarian cancer (OC)	MiR-137 and miR-34a act as Snail suppressors to negatively regulate EMT, invasive and sphere-forming properties of OC cells.	Downregulation	SKOV-3, ES-2, NOEC	Human	258
hsa-miR-137	MIMAT0000429	microRNA	30866999	2019	MicroRNA-137 reduces stemness features of pancreatic cancer cells by targeting KLF12	pancreatic cancer (PaCa)	MiR-137 is markedly downregulated in pancreatic cancer, contributing to tumor growth, invasion, and resistance to chemotherapy. MiR-137 upregulation dramatically decreased the size and number of spheres formed in AsPC-1 and PANC-1 cell cultures, while anti-miR-137 had the opposite effect. MiR-137 directly targets KLF12 and KLF12 activity contributes to the CSC phenotype in human pancreatic cancer cells.	Downregulation	AsPC-1, PANC-1	Human	259
hsa-miR-137	MIMAT0000429	microRNA	29975921	2018	MiR-137 Suppresses Triple-Negative Breast Cancer Stemness and Tumorigenesis by Perturbing BCL11A-DNMT1 Interaction	triple negative breast cancer (TNBC)	MiR-137 was significantly lower in both TNBC tissues and cell lines. Overexpression of miR-137 or knockdown of BCL11A reduced the number of tumoroshperes and the percentage of cancer stem cells in vitro, and inhibited tumor development in vivo.	Downregulation	MDA-MB-231, SUM149	Human	260
hsa-miR-141	MIMAT0000432	microRNA	30083271	2018	Carcinoma-associated fibroblasts promote the stemness and chemoresistance of colorectal cancer by transferring exosomal lncRNA H19	colorectal carcinoma (CRC)	H19 activated the beta-catenin pathway via acting as a competing endogenous RNA sponge for miR-141 in CRC, while miR-141 significantly inhibited the stemness of CRC cells. The mammosphere and tumor-initiating capacity of breast cancer cells were increased by knockdown of miR-141 74. Here, we found that the stemness of CRC cells was significantly suppressed by miR-141. The overexpression of miR-141 significantly decreased the sphere-forming capacities of SW480 and HCT116 cells, and the overexpression of miR-141 abolished the induction of ALDH1high cells by H19 overexpression.	Downregulation	SW480, HCT116	Human	263
hsa-miR-141	MIMAT0000432	microRNA	28535010	2017	MicroRNA-141 inhibits the self-renewal of glioblastoma stem cells via Jagged1	glioblastoma (GBM)	MiR-141 is suppressed in sorted cluster of differentiation (CD) 133+ glioblastoma stem cells (GSCs) compared with CD133(-) non-glioblastoma stem cells (NSCs) from patient samples. In addition, miR-141 overexpression inhibited the sphere formation ability of GSCs in vitro and in vivo.	Downregulation	glioblastoma stem cells (GSCs)	Human	264
hsa-miR-141-3p	MIMAT0000432	microRNA	27956179	2017	MiR-141-3p promotes prostate cancer cell proliferation through inhibiting kruppel-like factor-9 expression	prostate cancer (PCa)	MiR-141-3p is upregulated in prostate cancer cells and tissues compared to non-tumorigenic prostate epithelial cells and prostate tissues. MiR-141-3p positively regulated proliferation, spheroid formation, and expression of the stemness factors OCT-4, Nanog, SOX-9, Bmil, CCND1, and CD44 in PC-3 cells.	Upregulation	PC-3	Human	265
hsa-miR-142-5p	MIMAT0000433	microRNA	31724259	2020	BRD4 promotes glioma cell stemness via enhancing miR-142-5p-mediated activation of Wnt or beta-catenin signaling	glioma	BRD4 expression is increased in glioma tissues and negatively correlated with the overall survival of glioma patients. BRD4 promotes glioma cell stemness by analyzing ALDH1 activity, master stemness regulator expression, and sphere formation ability. Inhibition of miR-142-5p or reactivation of Wnt or beta-catenin signaling rescues the inhibition of BRD4 knockdown on glioma cell stemness.	Downregulation	U251, HS683	Human	269
hsa-miR-142-5p	MIMAT0000433	microRNA	34163033	2021	A novel homeostatic loop of sorcin drives paclitaxel-resistance and malignant progression via Smad4 or ZEB1 or miR-142-5p in human ovarian cancer	ovarian cancer (OC)	Our findings unveil a novel homeostatic loop of SRI that drives the PTX-resistance and malignant progression via Smad4 or ZEB1 or miR-142-5p in human OC. Targeting this SRI or Smad4 or ZEB1 or miR-142-5p loop may reverse the PTX-resistance.	Downregulation	OVCAR-3, SK-OV-3	Human	270
hsa-miR-142-3p	MIMAT0000434	microRNA	30091683	2018	miR-142-3p attenuates breast cancer stem cell characteristics and decreases radioresistance in vitro	breast cancer (BRCA)	Mammosphere formation was severely repressed in both generations after pre-miR-142-3p transfection. In the first generation, the reduction averaged more than 50percentage, whereas in the second generation, sphere formation declined by 80percentage compared to controls. MiR-142-3p downregulates cancer stem cell characteristics and radioresistance in breast cancer, mediated by a reduced role of beta-catenin in miR-142-3p-overexpressing cells.	Downregulation	MCF-7	Human	266
hsa-miR-142-3p	MIMAT0000434	microRNA	30741415	2019	miR-142-3p is a tumor suppressor that inhibits estrogen receptor expression in ER-positive breast cancer	breast cancer (BRCA)	MiR-142-3p is downregulated in ER-positive breast cancers. Restoration of miR-142-3p expression decreases stem cell features of ER-positive breast cancer cells.	Downregulation	MDA-MB-231, MCF-7	Human	267
hsa-miR-142-3p	MIMAT0000434	microRNA	30220706	2018	Exosomes from BM-MSCs increase the population of CSCs via transfer of miR-142-3p	colon cancer (CC)	Depriving miR-142-3p from BM-MSC-derived exosomes clearly decreased the population of colon CSCs. We selected miR-142-3p from the 50 microRNAs, as this was the only microRNA that promoted the formation of colon cancer (CC) stem-like spheres and the expression of CD133 and Lgr5 by FCM. Numb was found to be the target gene of miR-142-3p, and miR-142-3p promoted the Notch signalling pathway by downregulating Numb. BM-MSC-derived exosomes promote colon cancer (CC) stem cell-like traits via miR-142-3p.	Downregulation	HCT-116, HT-29, SW-480	Human	268
hsa-miR-143	MIMAT0000435	microRNA	28121625	2017	Cancer-associated fibroblasts release exosomal microRNAs that dictate an aggressive phenotype in breast cancer	breast cancer (BRCA)	Differential expression profile analysis identified three miRs (miRs -21, -378e, and -143) increased in exosomes from CAFs as compared from normal fibroblasts. Normal fibroblast exosomes transfected with miRs -21, -378e, and -144 promoted the stemness and EMT phenotype of breast cancer cells. Breast cancer cells (BT549, MDA-MB-231, and T47D lines) exposed to CAF exosomes or transfected with those miRs exhibited a significant increased capacity to form mammospheres, increased stem cell and epithelial-mesenchymal transition (EMT) markers, and anchorage-independent cell growth.	Upregulation	T47D, BT549, MDA-MB-231	Human	271
hsa-miR-143	MIMAT0000435	microRNA	23376635	2013	miR-143 inhibits glycolysis and depletes stemness of glioblastoma stem-like cells	glioblastoma (GBM)	We show that miR-143 is significantly down-regulated in glioma tissues and glioblastoma stem-like cells (GSLCs),while miR-143 over-expression inhibits glycolysis by directly targeting hexokinase 2, and promotes differentiation of GSLCs. Moreover, miR-143 inhibits proliferation of GSLCs under hypoxic conditions and decreases tumor formation capacity of GSLCs in vivo.	Downregulation	U87, GBM1	Human	272
hsa-miR-143-3p	MIMAT0000435	microRNA	32339330	2020	PCAT6 mediates cellular biological functions in gastrointestinal stromal tumor via upregulation of PRDX5 and activation of Wnt pathway	gastrointestinal stromal tumor (GIST)	MiR-143-3p was identified as the downstream microRNA of PCAT6. Further, sphere formation assay and Western blot revealed that miR-143-3p depletion or PRDX5 overexpression counteracted the suppressive effects of PCAT6 knockdown on cell stemness. Moreover, miR-143-3p itself served as a tumor suppressor in GIST. PCAT6 promoted GIST cell proliferation and stemness via sponging miR-143-3p to upregulate PRDX5.	Downregulation	GIST-882, GIST-T1	Human	273
hsa-miR-144	MIMAT0000436	microRNA	33308377	2020	A Preliminary Study of miR-144 Inhibiting the Stemness of colon cancer (CC) Stem Cells by Targeting Kruppel-Like Factor 4	colon cancer (CC)	MiR-144 was highly expressed in CRC cell lines and CSCs, and the overexpression of miR-144 in CSCs significantly promoted the proliferation of CSCs, inhibited its apoptosis, and promoted its invasion ability.	Upregulation	HCTI16	Human	274
hsa-miR-144	MIMAT0000436	microRNA	34333815	2023	MiR-144 or 451a cluster synergistically modulates growth and metastasis of Oral Carcinoma	oral squamous cell carcinoma (OSCC)	MiR-144 and miR-451a were downregulated in all cell lines. However, UPCI-SCC029B showed a significant reduction in cell viability for miR-451a, miR-144 or 451a, and miR-144-5p transfected cells but not for miR-144-3p transfected cells. MiR-144 or 451a cluster functions as a tumor suppressor in OSCC by inhibiting cancer cell invasion, migration, and clonogenic potential.	Downregulation	UPCI-SCC029B, UM-SCC083A	Human	275
hsa-miR-144-3p	MIMAT0000436	microRNA	35551606	2022	LINC00662 enhances cell progression and stemness in breast cancer by MiR-144-3p or SOX2 axis	breast cancer (BRCA)	The results of western blot showed that cleaved caspase 3 level was increased by LINC00662 depletion and then counteracted by miR-144-3p inhibition. In addition, sphere formation efficiency which was declined after LINC00662 knockdown, was then reversed by miR-144-3p knockdown. LINC00662 enhances cell proliferation, migration, invasion and stemness in BC by targeting miR-144-3p or SOX2 axis.	Downregulation	MDA-MB-231, MCF-7	Human	276
hsa-miR-144-3p	MIMAT0000436	microRNA	34657624	2021	MiR-144-3p inhibits gastric cancer progression and stemness via directly targeting GLI2 involved in hedgehog pathway	gastric cancer (GC)	MiR-144-3p was downregulated and served as an essential tumor suppressor in GC. As expected, the results showed that after transfected miR-144-3p mimics the tumorsphere formation ability of GCSCs was weakened and CD44 expression was decreased significantly. However, the tumorsphere formation ability was enhanced and CD44 expression was elevated after transfection with miR-144-3p inhibitor. Mechanistically, miR-144-3p inhibited gastric cancer progression and stemness by, at least in part, regulating GLI2 expression.	Downregulation	HGC-27, SGC-7901	Human	277
hsa-miR-145	MIMAT0000437	microRNA	29475734	2018	miR-145 Antagonizes SNAI1-Mediated Stemness and Radiation Resistance in Colorectal Cancer	colorectal carcinoma (CRC)	Using an in vitro spheroid formation assay, we evaluated SW620 cells after miR-145 transfection in a limiting dilution fashion. Our results showed that miR-145 significantly reduced spheroid formation in SW620 cells compared to scr control after transfection.	Downregulation	DLD1, HCT116	Human	278
hsa-miR-145	MIMAT0000437	microRNA	23312222	2013	MicroRNA miR-145 inhibits proliferation, invasiveness, and stem cell phenotype of an in vitro endometriosis model by targeting multiple cytoskeletal elements and pluripotency factors	endometriosis	MiR-145 inhibits endometriotic cell proliferation, invasiveness, and stemness by targeting multiple pluripotency factors, cytoskeletal elements, and protease inhibitors.	Downregulation	12Z	Human	279
hsa-miR-145	MIMAT0000437	microRNA	26374689	2016	Coordination of self-renewal in glioblastoma by integration of adhesion and microRNA signaling	glioblastoma (GBM)	CSCs expressed low levels of miR-145, and its introduction decreased self-renewal through reductions in AKT signaling and stem cell marker (SOX2, OCT4, and NANOG) expression. Indeed, introduction of miR-145 decreased the stem cell frequencies as well as the number of spheres formed.	Downregulation	293FT	Human	280
hsa-miR-145	MIMAT0000437	microRNA	22098779	2012	Inhibition of cancer stem cell-like properties and reduced chemoradioresistance of glioblastoma using microRNA145 with cationic polyurethane-short branch PEI	glioblastoma (GBM)	We found a similar pattern of miR145 downregulation and Sox2 or Oct4 upregulation in clinical biopsy tissues from patients with high-grade gliomas and GBMs relative to the mRNA levels in the samples from patients with lowgrade tumors. At the same time, these miR145-transfected GBM-CD133t cells lost their sphere-forming ability, miR145 transfection also caused the secondary and tertiary spheres to lose their sphereforming ability. We demonstrated that miR145 negatively regulates GBM tumorigenesis by targeting Oct4 and Sox2 in GBM-CD133+.	Downregulation	GBM cells	Human	281
hsa-miR-145	MIMAT0000437	microRNA	32339066	2020	Long noncoding RNA MACC1-AS1 promotes the stemness of hepatocellular carcinoma cells by antagonizing miR-145	hepatocellular carcinoma (HCC)	MiR-145 overexpression negatively regulated the expression of stemness master regulators, spheroid formation ability, and ALDH1 activity in clinical samples and cells in the same way that MACC1-AS1 did, and miR-145 expression was negatively correlated with MACC1-AS1 expression in clinical samples. MACC1-AS1 promoted the stemness of HCC cells by antagonizing miR-145 activity. Overexpression of miR-145 also attenuated HCC cell stemness.	Downregulation	SMMC7721, Huh7	Human	282
hsa-miR-145	MIMAT0000437	microRNA	29936107	2018	miR-145 mediates the anti-cancer stemness effect of photodynamic therapy with 5-aminolevulinic acid (ALA) in oral cancer cells	oral cancer	ALA-PDT upregulated the expression of microRNA-145 in two oral cancer cell lines. Overexpression of miR-145 in oral CSCs further enhanced the treatment effect of ALA-PDT with lower self-renewal, invasion capacities and reduced CD44 expression, while inhibition of miR-145 exhibited the opposite phenomena.	Downregulation	SAS, GNM	Human	283
hsa-miR-145	MIMAT0000437	microRNA	23404342	2013	Wild-type p53 suppresses the epithelial-mesenchymal transition and stemness in PC-3 prostate cancer cells by modulating miR-145	prostate cancer (PCa)	Anti-miR-145 restored the capability of tumor spheroid formation that was diminished by WT-p53 expression. Loss of WT-p53 might promote bone metastasis of PCa at least partially through repressing miR-145 to elevate EMT and stemness of cancer cells.	Downregulation	PC-3	Human	284
hsa-miR-145	MIMAT0000437	microRNA	22948942	2012	miR-143 and miR-145 inhibit stem cell characteristics of PC-3 prostate cancer cells	prostate cancer (PCa)	MiR-143 and miR-145 suppressed tumor sphere formation and expression of CSC markers and 'stemness' factors including CD133, CD44, Oct4, c-Myc and Klf4 in PC-4 cells.	Downregulation	PC-3	Human	285
hsa-miR-152	MIMAT0000438	microRNA	33090636	2021	Steroid receptor coactivator-1 enhances the stemness of glioblastoma by activating long noncoding RNA XIST or miR-152 or KLF4 pathway	glioblastoma (GBM)	SRC-1 promotes the stemness of GBM by activating the long noncoding RNA XIST or miR-152 or KLF4 pathway. MiR-152 reversed the expression of KLF4 and XIST, and that miR-152 mimic abolished the induced sphere-forming ability of SRC-1 or XIST in LN229-SRC1 cells.	Upregulation	LN229	Human	299
hsa-miR-152-3p	MIMAT0000438	microRNA	34336125	2021	Exosomal lncRNA PVT1 or VEGFA Axis Promotes colon cancer (CC) Metastasis and Stemness by Downregulation of Tumor Suppressor miR-152-3p	colon cancer (CC)	The subsequent addition of the miR-152-3p inhibitor significantly restored tumorsphere formation ability. PVT1, VEGFA, and EGFR interact with and are regulated by miR-152-3p. Increased miR-152-3p expression reduced tumorigenesis, where increased tumorigenesis was observed when miR-152-3p expression was downregulated.	Downregulation	HCT116, LoVo	Human	300
hsa-miR-153	MIMAT0000439	microRNA	23397238	2013	MicroRNA-153 is tumor suppressive in glioblastoma stem cells	glioblastoma (GBM)	QRT-PCR analysis showed that miR-153 expression was down-regulated in GBM tissues relative to normal brain tissues, and in CD133 positive cells relative to CD133 negative cells. After 7 days of culture, our results showed that miR-153 mimic transfected GBM-SCs generated a decreased number of secondary spheres. This project demonstrates for the first time that transient transfection of miR-153 into GBM-SCs can inhibit their stemness properties, such as impairing self-renewal ability and inducing differentiation. Meanwhile, miR-153 can also repress GBM-SCs growth and induce apoptosis.	Downregulation	GBM stem cells	Human	301
hsa-miR-153	MIMAT0000439	microRNA	26124081	2015	MicroRNA-153 or Nrf-2 or GPx1 pathway regulates radiosensitivity and stemness of glioma stem cells via reactive oxygen species	glioma	We found that microRNA (miR)-153 was down-regulated, miR-153 overexpression led to decreased neurosphere formation capacity, stem cell marker expression, and tumorigenic capacity.	Downregulation	U87, SHG44	Human	302
hsa-miR-153	MIMAT0000439	microRNA	32375892	2020	MiR-153 reduces stem cell-like phenotype and tumor growth of lung adenocarcinoma by targeting Jagged1	lung adenocarcinoma (LUAD)	MiR-153 expression was decreased in lung cancer tissues. Cells overexpressing miR-153 formed fewer and smaller tumor spheres than those transduced with the negative control. MiR-153 suppresses the stem cell-like phenotypes and tumor growth of lung adenocarcinoma by targeting Jagged1.	Downregulation	SPC-A-1	Human	303
hsa-miR-153	MIMAT0000439	microRNA	26941846	2016	Mifepristone Suppresses Basal Triple-Negative Breast Cancer Stem Cells by Down-regulating KLF5 Expression	triple negative breast cancer (TNBC)	MIF suppresses the expression of KLF5 through inducing the expression of miR-153. Consistently, miR-153 decreases CSC and miR-153 inhibitor rescued MIF-induced down-regulation of the KLF5 protein level and CSC ratio. Importantly, miR-153 significantly decreased the CSC population of HCC1937 by both the CD24 or CD44 analysis, the Aldefluor assay, and the mammosphere formation assay.	Downregulation	MCF10A, HCC1937	Human	304
hsa-miR-9	MIMAT0000441	microRNA	28062574	2017	Loss of N-Acetylgalactosaminyltransferase-4 Orchestrates Oncogenic MicroRNA-9 in Hepatocellular Carcinoma	hepatocellular carcinoma (HCC)	Performing a series of functional studies, we found that suppression of endogenous miR-9 expression by anti-miR-9 strongly inhibited sphere-forming ability. A luciferase activity assay further identified microRNA-9 (miR-9) as the crucial specific arbitrator for GALNT4 expression in HCC cells. Furthermore, restoring GALNT4 expression attenuates miR-9-mediated oncogenic functions. GALNT4 expression is markedly repressed in primary HCC tissues, and reduced expression of GALNT4 is significantly associated with adverse survival of patients with HCC.	Upregulation	Huh7, SK-Hep1	Human	565
hsa-miR-9	MIMAT0000441	microRNA	30110679	2018	Increased Cellular Levels of MicroRNA-9 and MicroRNA-221 Correlate with Cancer Stemness and Predict Poor Outcome in Human Breast Cancer	breast cancer (BRCA)	Knockdown of both miR-9 and miR-221 in invasive MDA-MB-232 breast cancer cells dramatically decreased the number of side-population colonies with stem cell-like potency, which reduced the capacity for tumor-cell renewal, invasion, and migration. Upon transfection of cells with both miRNA inhibitors, the number of tumorsphere-forming MDA-MB-231 cells was reduced by > 80percentage together with a reduction in the transcription of the stemness markers CD133, Nanog, and Oct4 genes.	Upregulation	MCF-7, MDA-MB-231	Human	566
hsa-miR-9-5p	MIMAT0000441	microRNA	32482375	2020	The long noncoding RNA EMBP1 inhibits the tumor suppressor miR-9-5p and promotes renal cell carcinoma tumorigenesis	renal cell carcinoma (RCC)	Moreover, since the acquisition of EMT is shown to be mechanistically linked with a CSC-like phenotype, we also analyzed the expression of the stemness markers KLF4 and Nanog under miR-9-5p-overexpression conditions. We observed a decrease in KLF4 and Nanog protein levels in both ACHN and Caki-1 cell lines as compared with control, suggesting reduced stemness with miR-9-5p overexpression. MiR-9-5p was significantly down-regulated, and EMBP1 was significantly up-regulated, in RCC cell lines and tumor tissue. Overexpression of miR-9-5p or EMBP1 suppression in RCC cell lines significantly retarded their proliferative, migratory, and invasive behavior, in addition to promoting apoptosis and cell-cycle arrest.	Downregulation	ACHN, Caki-1	Human	573
hsa-miR-127	MIMAT0000446	microRNA	27869168	2017	miR-127 promotes EMT and stem-like traits in lung cancer through a feed-forward regulatory loop	lung cancer (LC)	We revealed that, in comparison with their parental cells, miR-127-expressing PC9 cells exhibited an increase in sphere-like aggregates, whereas miR-127-silenced A549 cells profoundly reduced cell spheroids formation. Elevated miR-127 level drove a pronounced shift from the epithelial to the mesenchymal phenotype in cancer cells, and this shift was associated with their acquisition of stem-like traits, increased resistance to the epidermal growth factor receptor inhibitor and tumor-propagating potential.	Upregulation	PC9, A549	Human	237
hsa-miR-127-3p	MIMAT0000446	microRNA	34431063	2021	Mesenchymal stem cell-derived exosomes block malignant behaviors of hepatocellular carcinoma stem cells through a lncRNA C5orf66-AS1 or microRNA-127-3p or DUSP1 or ERK axis	hepatocellular carcinoma (HCC)	In the setting of miR-127-3p upregulation, it was found that the proliferation ability of CSCs, which was initially suppressed by Exo, was recovered. Likewise, the colony formation ability of the CSCs was restored after miR-127-3p overexpression. In addition, the wound healing and Transwell assay results indicated the migration and invasion potentials of CSCs were restored after miR-127-3p overexpression.	Upregulation	HuH7, Hep3B	Human	238
hsa-miR-134	MIMAT0000447	microRNA	24440911	2014	Multiple receptor tyrosine kinases converge on microRNA-134 to control KRAS, STAT5B, and glioblastoma	glioblastoma (GBM)	We find that miR-134 is downregulated in human tumors and cancer stem cells and that its expression inversely correlates with the activation of MET, EGFR, and PDGFR. We demonstrate that miR-134 inhibits cancer cell and stem-cell proliferation, survival, and xenograft growth, as well as cancer stem-cell self-renewal and stemness.	Downregulation	U373, U87	Human	253
hsa-miR-146a	MIMAT0000449	microRNA	30056535	2018	Fascin protein stabilization by miR-146a implicated in the process of a chronic inflammation-related colon carcinogenesis model	colon cancer (CC)	MiR-146a was upregulated in FPCKpP1-4 adenocarcinoma cells. MiR-146a in the adenocarcinoma cells brought about acquisition of sphere formation, cancer stemness, and inhibition of proteasomal degradation of the fascin protein.	Upregulation	FPCK-1-1, FPCKpP1-4	Human	286
hsa-miR-146a	MIMAT0000449	microRNA	32973101	2021	A Novel miR-146a-POU3F2 or SMARCA5 Pathway Regulates Stemness and Therapeutic Response in Glioblastoma	glioblastoma (GBM)	MiR-146a level was significantly lower in recurrent tumors compared with primary ones. Notably, we observed that overexpression of miR-146a in primary GBM cells significantly inhibited sphere formation, a characteristic feature of these cells. Similarly, miR-146a overexpression reduced sphere formation frequency and sphere size by in vitro limiting dilution and sphere formation assays, as well as in vivo tumorigenicity by frequency of tumor-initiating cells (TICf), indicating that overexpression of miR-146a inhibited expansion of GSCs. MiR-146a-POU3F2 or SMARCA5 pathway plays a critical role in suppressing GBM-stemness and increasing TMZ-response.	Downregulation	LN229, U87, LN18	Human	288
hsa-miR-149-5p	MIMAT0000450	microRNA	35864972	2022	YY1-induced DLEU1 or miR-149-5p Promotes Malignant Biological Behavior of cholangiocarcinoma (CCA) through Upregulating YAP1 or TEAD2 or SOX2	cholangiocarcinoma (CCA)	The results confirmed that upregulated miR-149-5p restrained proliferation, invasion, and stemness maintenance of CCA cells, whereas knocking down miR-149-5p promoted cellular proliferation, invasion, and stemness maintenance. DLEU1 promoted oncogene YAP1 expression by functioning as a sponge to competitively bind to miR-149-5p. MiR-149-5p inhibited malignant biological behavior of CCA. YY1-mediated DLEU1 upregulated YAP1 via sponging miR-149-5p, thereby boosting CCA development.	Downregulation	RBE, HCCC-9810, QBC939, CCLP-1, HIBEC	Human	296
hsa-miR-149-5p	MIMAT0000450	microRNA	31855318	2020	The miRNA-149-5p or MyD88 axis is responsible for ursolic acid-mediated attenuation of the stemness and chemoresistance of non-small cell lung cancer cells	non-small cell lung cancer (NSCLC)	Mechanistic investigations revealed that UA inhibited the miR-149-5p or MyD88 signaling, which is responsible for UA-mediated effects on the stemness of A549-PR cells.MiR-149-5p or MyD88 axis promoted the stemness of A549 cells, while inhibition of this axis attenuated the stemness of A549-PR cells.	Upregulation	A549	Human	297
hsa-miR-185-5p	MIMAT0000455	microRNA	34870557	2022	LncRNA ASB16-AS1 drives proliferation, migration, and invasion of colorectal cancer cells through regulating miR-185-5p or TEAD1 axis	colorectal carcinoma (CRC)	Moreover, the results of sphere formation assays demonstrated that miR-185-5p overexpression declined the sphere formation efficiency. Meanwhile, OCT4, Nanog, and SOX2 expressions at mRNA level and protein level were all reduced after the overexpression of miR-185-5p.	Downregulation	LOVO, HT-29	Human	320
hsa-miR-186-5p	MIMAT0000456	microRNA	32390141	2020	LncRNA TUG1 facilitates proliferation, invasion and stemness of ovarian cancer cell via miR-186-5p or ZEB1 axis	ovarian cancer (OC)	The silencing of TUG1 and upregulation of miR-186-5p both suppressed the cell proliferation, invasion and cancer stem cell (CSC) properties. TUG1 sponges miR-186-5p to release ZEB2 and promotes the proliferation, invasion and stemness of OC cells.	Downregulation	A2780, SKOV3	Human	321
hsa-miR-194	MIMAT0000460	microRNA	31960990	2020	Upregulated microRNA-194 impairs stemness of cholangiocarcinoma (CCA) cells through the Rho pathway via inhibition of ECT2	cholangiocarcinoma (CCA)	ECT2 was highly expressed while miR-194 was poorly expressed in CCA stem cells.MiR-194 inhibits ECT2 and blocks the activation of Rho signaling pathway, thus promoting apoptosis, inhibiting proliferation and migration of CCA stem cells, and suppressing tumor growth.	Downregulation	QBC-939	Human	323
hsa-miR-195-5p	MIMAT0000461	microRNA	29852230	2018	Overcoming stemness and chemoresistance in colorectal cancer through miR-195-5p-modulated inhibition of notch signaling	colorectal carcinoma (CRC)	MiR-195-5p expression was significantly decreased as compared to paired, tumor-adjacent normal colorectal tissues. MiR-195-5p significantly increased cancer cell apoptosis and decreased tumor sphere formation. The 3' UTR of Notch signaling proteins Notch2 and RBPJ, which are essential genes in CRC cell stemness and chemoresistance, possessed double putative binding sites of miR-195-5p.	Downregulation	SW620, HT-29	Human	324
hsa-miR-206	MIMAT0000462	microRNA	27435395	2017	miR-206 Inhibits Stemness and Metastasis of Breast Cancer by Targeting MKL1 or IL11 Pathway	breast cancer (BRCA)	MiR-206 suppresses breast tumor stemness and metastasis by inhibiting both self-renewal and invasion. MKL1 and SRF were further demonstrated to promote the expression of IL11, which is essential for miR-206's function in inhibiting both invasion and stemness of breast cancer.	Downregulation	MCF-7	Human	363
hsa-miR-206	MIMAT0000462	microRNA	32771526	2020	HOTAIR maintains the stemness of ovarian cancer stem cells via the miR-206 or TBX3 axis	ovarian cancer (OC)	Moreover, RT-qPCR confirmed the reduced expression of miR-206 in ALDHbr cells and OVCAR3 spheres compared with that of ALDHdi or parent OVCAR3 cells. MiR-206 expression was effectively regulated by the designed mimic and inhibitor. MiR-206 inhibited the expression of TBX3 and NANOG, but induced PTEN expression. Functionally, the sphere-formation ability of ALDHbr cells was inhibited after miR-206 mimic transfection, whereas inhibition of miR-206 increased the sphere formation ability in OVCAR3 cells.	Downregulation	SKOV3, ES2, OVCAR3	Human	364
hsa-miR-320a	MIMAT0000510	microRNA	29971915	2018	Long non-coding RNA AFAP1-AS1 or miR-320a or RBPJ axis regulates laryngeal carcinoma cell stemness and chemoresistance	laryngeal carcinoma (LC)	To explore the possible role of miR-320a in laryngeal carcinoma cell stemness, we performed qRT-PCR to detect miR-320a expression between parental cells and stemness-enriched cell spheres. We found that miR-320a was down-regulated in cell spheres. To further explore miR-320a function in laryngeal carcinoma cell development, we increased miR-320a expression by miR-320a transfection, confirming miR-320a overexpression by qRT-PCR. qRT-PCR of these cells then revealed that expression levels of stemness-associated genes were significantly reduced in miR-320a overexpression cells as compared to miR-control cells. Tumour sphere assays then showed that AFAP1-AS1 overexpression moderately inhibited cell self-renewal. These results indicate that miR-320a overexpression reduces laryngeal carcinoma cell stemness while increasing chemosensitivity to cisplatin.	Downregulation	HEp-2	Human	424
mmu-miR-148a	MIMAT0000516	microRNA	27779717	2016	miR-148a inhibits self-renewal of thyroid cancer stem cells via repressing INO80 expression	anaplastic thyroid carcinoma (ATC)	Overexpression of miRNA-148a and knockdown of INO80 acted synergistically to decrease the expression of stem cell marker genes as well as to attenuate stem cell-specific properties including the ability to form tumors.	Downregulation	p20	Mouse	290
mmu-miR-196a	MIMAT0000518	microRNA	27880730	2016	Loss of ZG16 is regulated by miR-196a and contributes to stemness and progression of colorectal cancer	colorectal carcinoma (CRC)	The upstream regulator of ZG16, miR-196a, which was significantly overexpressed in CRC and promotes cell growth and stemness. Moreover, overexpression of miR-196a also promotes the sphere forming ability of LGR5- CRC cells and increased the LGR+ CRC cell population.	Upregulation	HT29	Mouse	325
mmu-miR-34a	MIMAT0000542	microRNA	27082152	2016	The influence of miR-34a expression on stemness and cytotoxic susceptibility of breast cancer stem cells	breast cancer (BRCA)	MiR-34a could separately reduce the stemness of BCSCs and activate the cytotoxic susceptibility of BCSCs to natural killer (NK) cells in vitro via down regulating the expression of Notch1 signaling molecules. Moreover, miR-34a could completely restrain established mice breast tumor xenografts in vivo in the NOD or SCID mice that have functional NK cells at a normal level, whereas it was less effective in NOD or SCID or CD122 or IL-2Rbeta mice that do not have functional NK cells.	Downregulation	4T1	Mouse	447
mmu-miR-135b	MIMAT0000612	microRNA	23623609	2013	miR-135b coordinates progression of ErbB2-driven mammary carcinomas through suppression of MID1 and MTCH2	breast cancer (BRCA)	MiR-135b silencing significantly reduced mammosphere generation in a sphere generation assay. MiR-135b silencing significantly reduced mammosphere generation in a sphere generation assay.	Upregulation	TUBO, TSA, 4T1	Mouse	255
hsa-miR-200c	MIMAT0000617	microRNA	32019566	2020	Long non-coding RNA SOX2OT promotes the stemness phenotype of bladder cancer cells by modulating SOX2	bladder cancer (BLCA)	SOX2OT was highly expressed in bladder cancer. Knockdown of SOX2OT inhibited the stemness phenotype of BCSCs, and inhibition of SOX2OT delayed xenograft tumour growth and decreased metastases in vivo. Knockdown of miR-200c significantly reversed the spheroid-formation ability inhibition induced by silencing SOX2OT.	Upregulation	SW780, 5637	Human	340
hsa-miR-200c	MIMAT0000617	microRNA	26400441	2015	Essential role of miR-200c in regulating self-renewal of breast cancer stem cells and their counterparts of mammary epithelium	breast cancer (BRCA)	MiRNA-200c is downregulated in both MaSCs and BCSCs. From seeding cells of the same number, MaSCs transfected with miR-200c agomir resulted in significantly fewer mammospheres, and miR-200c antagomir significantly increased mammospheres than those transfected with miR-control. The similar result was found in BCSC experiment. BCSCs transfected with miR-200c agomir resulted in significantly fewer mammospheres than those transfected with miR-control. In contrast, miR-200c antagomir significantly increased mammospheres. In gain- and lost-of-function assays, miR-200c was sufficient to inhibit the self-renewal of BCSCs and MaSCs in vitro and the growth of BCSCs in vivo.	Downregulation	MCF-10A	Human	341
hsa-miR-200c	MIMAT0000617	microRNA	31599500	2019	miR-200c suppresses stemness and increases cellular sensitivity to trastuzumab in HER2+ breast cancer	breast cancer (BRCA)	MiR-200c was weakly expressed in breast cancer cell lines and cell line stem cells. Overexpression of miR-200c resulted in a significant reduction in the number of tumour spheres formed and the population of CD44+ CD24- phenotype mammospheres in SKBR3-S.	Downregulation	MCF-7, SKBR3	Human	342
hsa-miR-200c	MIMAT0000617	microRNA	34312289	2021	Mutant p53 Attenuates Oxidative Phosphorylation and Facilitates Cancer Stemness through Downregulating miR-200c-PCK2 Axis in Basal-Like Breast Cancer	breast cancer (BRCA)	Our results suggest that p53 and miR-200c regulate OXPHOS and stem or cancer stemness through PCK2, and loss of the p53-miR-200c-PCK2 axis might provide metabolic advantages that facilitate cancer stemness, leading to the progression of BLBCs.	Downregulation	MCF12A, BT549, MDA-MB-231	Human	343
hsa-miR-200c	MIMAT0000617	microRNA	33673143	2021	miR-34a and miR-200c Have an Additive Tumor-Suppressive Effect on Breast Cancer Cells and Patient Prognosis	breast cancer (BRCA)	MiR-34a and miR-200c levels are reduced in breast tumors compared to adjacent normal tissues and that this additively predicts poor patient survival. MiR-34a and miR-200c additively induce apoptosis and cell cycle arrest, while also inhibiting proliferation, invasion, migration, stemness and epithelial-to-mesenchymal transition (EMT).	Downregulation	MDA-MB-231, MCF-7	Human	344
hsa-miR-200c	MIMAT0000617	microRNA	24658157	2014	Regulation of colorectal carcinoma stemness, growth, and metastasis by an miR-200c-Sox2-negative feedback loop mechanism	colorectal carcinoma (CRC)	MiR-200c was statistically lower in CRC clinical specimens and highly metastatic CRC cell lines compared with their counterparts. The knockdown of miR-200c significantly enhanced proliferation, migration, and invasion in CRC cell lines, whereas the upregulation of miR-200c exhibited an inverse effect. In addition, the reduction of miR-200c increased the expression of CRC stem cell markers and the sphere-forming capacity of CRC cell lines.	Downregulation	SW480, HCT116	Human	345
hsa-miR-200c-3p	MIMAT0000617	microRNA	32617772	2021	Inhibition of MicroRNA-302c on Stemness of colon cancer (CC) Stem Cells via the CARF or Wnt or beta-Catenin Axis	colon cancer (CC)	The expression of miR-302c in CC cells was reduced versus that in normal cells. The overexpression of miR-302c weakened the stemness, proliferation, invasion, and migration abilities while induced apoptosis of CSCs in CC. Also, miR-302c reduced tumor size and weight in mice, accompanied with lowered CARF expression. The mechanistic analysis manifested that miR-302c bound to CARF and suppressed its expression and disrupted the Wnt or beta-catenin signaling.	Downregulation	SW1116, SW480	Human	346
hsa-miR-155	MIMAT0000646	microRNA	32096299	2020	miR-155 increases stemness and decitabine resistance in triple-negative breast cancer cells by inhibiting TSPAN5	triple negative breast cancer (TNBC)	MiR-155 was upregulated in CD24- CD44+ BC stem cells (BCSCs). MiR-155 increases stemness and DCA resistance in BC cells by targeting TSPAN5.	Upregulation	MDA-231, BT-549	Human	306
hsa-miR-106b-5p	MIMAT0000680	microRNA	28423523	2017	miR-106b-5p promotes renal cell carcinoma aggressiveness and stem-cell-like phenotype by activating Wnt or beta-catenin signalling	clear cell renal cell carcinoma (ccRCC)	We can see that the size and numbers of spheres increased in miR-106b-5p overexpression A498 cells and decreased in miR-106b-5p knockdown Caki-1 cells. ccRCC cells and tissues expressed more miR-106b-5p than normal controls. Gain- and loss-of-function studies demonstrated that overexpression of miR-106b-5p in ccRCC cells increased the spheres formation ability and the proportion of side population cells. MiR-106b-5p mediates the constitutive activation of Wnt or beta-catenin signalling.	Upregulation	A498, HK-2, Caki-1	Human	215
hsa-miR-106b-5p	MIMAT0000680	microRNA	35364458	2022	HNRNPA2B1 inhibited SFRP2 and activated Wnt-beta or catenin via m6A-mediated miR-106b-5p processing to aggravate stemness in lung adenocarcinoma	lung adenocarcinoma (LUAD)	Sphere size formed by LUAD cells and ratio of CD133 + LUAD cells decreased by HNRNPA2B1 was recovered by miR-106b-5p mimics, and such recovery was abrogated by SFRP2 over expression. HNRNPA2B1 inhibits SFRP2 and activates Wnt-beta or catenin via m6A-mediated maturing of miR-106b-5p to aggravate stemness and LUAD progression.	Upregulation	A549, H1975	Human	216
hsa-miR-302a	MIMAT0000684	microRNA	30326936	2018	MicroRNA-302a or d inhibits the self-renewal capability and cell cycle entry of liver cancer stem cells by targeting the E2F7 or AKT axis	hepatocellular carcinoma (HCC)	E2F7 is a direct target of miRNA-302a or d and miRNA-302a or d inhibits the stemness of LCSCs and proliferation of HCC cells by targeting the E2F7 or AKT or beta-catenin or CCND1 signaling pathway. The spheroid formation and cellular growth assay revealed that following miRNA-302a or d overexpression, the spheroid formation and growth rate of HepG2 and Huh7 cells were significantly inhibited when compared to the control group.	Downregulation	HepG2, Huh7	Human	414
hsa-miR-34C	MIMAT0000686	microRNA	27461446	2016	miR-34C Disrupts the Stemness of Purified CD133+ Prostatic Cancer Stem Cells	prostate cancer (PCa)	We identified that miR-34C was under-expressed in the purified CD133+ PCSCs and enforced introduction of miR-34C attenuated the stemness of CD133+ PCSCs.	Downregulation	LNCaP, C4-2	Human	459
hsa-miR-34c-5p	MIMAT0000686	microRNA	35866307	2022	Loss of exosomal miR-34c-5p in cancer-associated fibroblast for the maintenance of stem-like phenotypes of laryngeal cancer cells	laryngeal squamous cell carcinoma (LSCC)	MiR-34c-5p expression is significantly reduced in CAF-derived exosomes. The sphere formation assays showed that the cancer cells cultured with exo-miR-34c-5p formed the fewest number and the smallest size of spheres. The cancer cells cultured with exo-miR-NC and exo-control formed more and larger spheres, and the differences in the number and size of spheres was significant compared with the cells cultured alone. Loss of miR-34c-5p in CAF-derived exosomes contributes to the maintenance of stem-like phenotypes of LSCC.	Downregulation	AMC-HN-8, FD-LSC-1	Human	460
hsa-miR-299-3p	MIMAT0000687	microRNA	36260520	2022	Matrine induces hepatocellular carcinoma apoptosis and represses EMT and stemness through microRNA-299-3p or PGAM1 axis	hepatocellular carcinoma (HCC)	Moreover, the impacts of miR-299-3p inhibition on EMT markers (E-cadherin, N-cadehrin, etc.) and EMT-tf markers, as well as on Sox2, Oct4 and Nanog expression and tumour sphere formation were also be saved by interfering with PGAM1. Matrine elevated miR-299-3p expression, repressed proliferation, invasion, and anti-apoptosis of HCC cells, and constrained EMT and stemness in vitro.	Downregulation	MHCC-97H	Human	408
hsa-miR-296-5p	MIMAT0000690	microRNA	26898758	2016	Epigenetic modulation of a miR-296-5p:HMGA1 axis regulates Sox2 expression and glioblastoma stem cells	glioblastoma (GBM)	Inhibition of endogenous miR-296-5p concurrently increased self-renewal as evidenced by significant increases in the number and size of neurospheres and consistently increased the expression of SC drivers Sox2, the pluripotency transcription factor Nanog and stem cell markers Nestin and Olig2.	Downregulation	A172	Human	405
hsa-miR-296-5p	MIMAT0000690	microRNA	32320856	2020	miR-296-5p suppresses stem cell potency of hepatocellular carcinoma cells via regulating Brg1 or Sall4 axis	hepatocellular carcinoma (HCC)	MiR-296-5p exerts an inhibitory effect on stemness potency of HCC cells via Brg1 or Sall4 axis. MiR-296-5p was able to inhibit the stemness potency of HCC by decreasing the number and size of tumorspheres, downregulating the expression of CSC biomarkers and hampering the ability of tumorigenesis in NOD or SCID mice.	Downregulation	MHCC97H, Huh7	Human	406
hsa-miR-363-3p	MIMAT0000707	microRNA	30784290	2019	MicroRNA-363-3p or p21(Cip1 or Waf1) axis is regulated by HIF-2alpha in mediating stemness of melanoma cells	melanoma	The levels of miR-363-3p and HIF-2alpha were upregulated in melanoma cell lines. MiR-363-3p is induced by HIF-2alpha to promote the stemness of melanoma cells via inhibiting p21.	Upregulation	A2058, WM793B	Human	461
hsa-miR-302b	MIMAT0000715	microRNA	22384170	2012	Ascl2 knockdown results in tumor growth arrest by miRNA-302b-related inhibition of colon cancer (CC) progenitor cells	colon cancer (CC)	Restoration of miRNA-302b, via its mimic, led to the restoration of shRNA-Ascl2 or HT-29 'stemness' characteristics, including tumorsphere formation and 'stemness' associated genes levels, and the recovery of cellular behaviors, including colony-forming ability, invasion and migration in vitro.	Upregulation	HT-29, LS174T	Human	415
hsa-miR-302c-5p	MIMAT0000716	microRNA	36539366	2022	MiR-302c-5p affects the stemness and cisplatin resistance of nasopharyngeal carcinoma cells by regulating HSP90AA1	nasopharyngeal carcinoma (NPC)	The expression of miR-302c-5p was substantially reduced and HSP90AA1 was increased in NPC cells. At the same time, the overexpression of miR-302c-5p in the miR-302c-5p mimic group reduced the number of cancer cell spheres and size of NPC cells. Inhibition of miR-302c-5p increased the number of cancer cell spheres and the size of NPC cells. Additionally, miR-302c-5p inhibited cisplatin resistance and the traits of stem cells in NPC.	Downregulation	CNE2, 5-8F	Human	416
hsa-miR-302d	MIMAT0000718	microRNA	30326936	2018	MicroRNA-302a or d inhibits the self-renewal capability and cell cycle entry of liver cancer stem cells by targeting the E2F7 or AKT axis	hepatocellular carcinoma (HCC)	E2F7 is a direct target of miRNA-302a or d and miRNA-302a or d inhibits the stemness of LCSCs and proliferation of HCC cells by targeting the E2F7 or AKT or beta-catenin or CCND1 signaling pathway. The spheroid formation and cellular growth assay revealed that following miRNA-302a or d overexpression, the spheroid formation and growth rate of HepG2 and Huh8 cells were significantly inhibited when compared to the control group.	Downregulation	HepG2, Huh7	Human	417
hsa-miR-367	MIMAT0000719	microRNA	31402560	2019	miR-367 as a therapeutic target in stem-like cells from embryonal central nervous system tumors	embryonal CNS tumor	OCT4A overexpression has been shown to up-regulate miR-367. MiR-367 silencing in OCT4A-overexpressing tumor cells significantly reduced their proliferative and invasive behavior, clonogenic activity, and tumorsphere generation capability.	Upregulation	USP13-MED, USP7-ATRT	Human	463
hsa-miR-370-3p	MIMAT0000722	microRNA	33629796	2021	MicroRNA-370-3p shuttled by breast cancer cell-derived extracellular vesicles induces fibroblast activation through the CYLD or Nf-kappaB axis to promote breast cancer progression	breast cancer (BRCA)	EVs-derived miR-370-3p activated the NFs to promote the enhancement of stemness, migration, and invasion and EMT of breast cancer cells in vitro. Our results showed that the expression of stem cell markers CD133, OCT4, NANOG, and CD90 in MCF-7 cells was reduced and sphere formation, migratory, and invasive ability were weakened following 231-EV_miR-370-3p inhibitor treatment, when compared to treatment with 231-EV_inhibitor-NC.	Upregulation	MCF-7	Human	464
hsa-miR-372	MIMAT0000724	microRNA	30171794	2018	miR-372 and miR-373 enhance the stemness of colorectal cancer cells by repressing differentiation signaling pathways	colorectal carcinoma (CRC)	The upregulation in expression of miR-372 or 373 in CRC tissues from The Cancer Genome Atlas data, and overexpression of miR-372 or 373 enhanced the stemness of CRC cells by enriching the CD26 or CD24-positive cell population and promoting self-renewal, chemotherapy resistance and the invasive potential of CRC cells. MiR-372 or 373 enhance CRC cell stemness by repressing the expression of differentiation genes.	Upregulation	HCT116, RKO	Human	466
hsa-miR-373	MIMAT0000726	microRNA	30171794	2018	miR-372 and miR-373 enhance the stemness of colorectal cancer cells by repressing differentiation signaling pathways	colorectal carcinoma (CRC)	The upregulation in expression of miR-372 or 373 in CRC tissues from The Cancer Genome Atlas data, and overexpression of miR-372 or 373 enhanced the stemness of CRC cells by enriching the CD26 or CD24-positive cell population and promoting self-renewal, chemotherapy resistance and the invasive potential of CRC cells. MiR-372 or 373 enhance CRC cell stemness by repressing the expression of differentiation genes.	Upregulation	HCT116, RKO	Human	467
hsa-miR-374a	MIMAT0000727	microRNA	30032142	2018	MicroRNA-374a Inhibits Aggressive Tumor Biological Behavior in Bladder Carcinoma by Suppressing Wnt or beta-Catenin Signaling	bladder cancer (BLCA)	MiR-374a mimic could block the Wnt or beta-catenin signaling pathway to regulate different tumor behaviors, including metastasis, invasion, cancer stemness, apoptosis, and drug resistance. MiR-374a mimic abrogated the metastatic potential and invasiveness of bladder cancer cells via WNT5A downregulation in both T24 and TCCSUP human bladder cancer cells.	Downregulation	T24, TCCSUP	Human	468
hsa-miR-375	MIMAT0000728	microRNA	32738343	2020	MiR-375 inhibits the stemness of breast cancer cells by blocking the JAK2 or STAT3 signaling	breast cancer (BRCA)	MiR-375 not only reduced the stemness, but also decreased adriamycin resistance of breast cancer cells. These results were characterized by the decrease of BCSC rate, mammosphere-forming and tumor-initiating ability, and IC50 value of adriamycin, and weakened by JAK2 re-expression. MiR-375 suppresses the stemness of breast cancer cells through targeting JAK2.	Downregulation	MCF-7, MDA-MB-231, MCF-7 or ADR	Human	469
hsa-miR-375	MIMAT0000728	microRNA	36190453	2023	CircRPPH1 promotes the stemness of gastric cancer cells by targeting miR-375 or SLC7A11 axis	gastric cancer (GC)	In addition, both miR-375 inhibition and SLC7A11 overexpression attenuated the inhibitory effects of circRPPH1 knockdown on the sphere-formation ability of GC cells. CircRPPH1 acted as an miR-375 sponge to positively regulate SLC7A11 expression, which has been confirmed to be the direct target of miR-375 in gastric cancer, and thus regulated ferroptosis. Moreover, circRPPH1 promoted the stemness of gastric cancer cells dependent on the miR-375 or SLC7A12.	Downregulation	MKN-46, AGS	Human	470
hsa-miR-375	MIMAT0000728	microRNA	34090492	2021	MiR-375 reduces the stemness of gastric cancer cells through triggering ferroptosis	gastric cancer (GC)	MiR-375 can trigger the ferroptosis through targeting SLC7A11, which could provoke the ferroptosis and thus attenuate the stemness of GC cells.	Downregulation	SGC-7901, BGC-823	Human	471
hsa-miR-376a	MIMAT0000729	microRNA	30909144	2019	RNA binding protein PUM2 promotes the stemness of breast cancer cells via competitively binding to neuropilin-1 (NRP-1) mRNA with miR-376a	breast cancer (BRCA)	PUM2 competitively bound to NRP 3'UTR with miR-376a, which had been previously confirmed by us to suppress the stemness of breast cancer cells, and increased NRP-1 mRNA stability and expression. PUM2 could facilitate the stemness of breast cancer cells by competitively binding to NRP-1 3'UTR with miR-376a.	Downregulation	MDA-MB-231,MDA-MB-453	Human	472
hsa-miR-378a-3p	MIMAT0000732	microRNA	33823894	2021	Chemotherapy-elicited exosomal miR-378a-3p and miR-378d promote breast cancer stemness and chemoresistance via the activation of EZH2 or STAT3 signaling	breast cancer (BRCA)	To investigate the function of exosome-derived miR-378a-3p and miR-378d, CAL51 and MDA-MB-231 cells were transfected with miR-378a-3p and miR-378d mimics or negative control (NC), and post-transfection cells were subjected to drug sensitivity assays, CD44+ or CD24- population analyses and sphere formation assays. MiR-378a-3p and miR-378d were found to contribute to the decreased drug sensitivity of cells to DOX and PTX and increased percentage of cancer stem cells. Similar results were obtained with MCF7 cells. Chemotherapy-elicited exosomal miR-378a-3p and miR-378d regulate the WNT or beta-catenin and Notch stemness pathways by targeting NUMB and DKK3.	Upregulation	CAL51, MDA-MB-231, MCF-7	Human	473
hsa-miR-378a-3p	MIMAT0000732	microRNA	36245214	2022	MiR-378a-3p acts as a tumor suppressor in gastric cancer via directly targeting RAB31 and inhibiting the Hedgehog pathway proteins GLI1 or 2	gastric cancer (GC)	MiR-378a-3p is downregulated in GC, whereas its overexpression inhibits proliferation, invasion, and migration as well as promotes apoptosis in GC cells. As expected, the tumorsphere formation ability of GCSCs was significantly attenuated after transfection with miR-378a-3p mimics, whereas the tumorsphere formation ability was enhanced after transfection with miR-378a-3p inhibitor. MiR-378a-3p inhibits GLI1 or 2 in the Hedgehog signaling pathway and attenuates the stemness of gastric cancer stem cells. Xenograft assays showed that miR-378a-3p inhibits GC tumorigenesis in vivo.	Downregulation	BGC-823, SGC-7901	Human	474
hsa-miR-340	MIMAT0000750	microRNA	32005118	2020	Hsa_circ_001680 affects the proliferation and migration of CRC and mediates its chemoresistance by regulating BMI1 through miR-340	colorectal carcinoma (CRC)	The results of the sphere formation assay demonstrated that the circ_001680-overexpressing cells could form more viable spheres, whereas the number of spheres was significantly reduced through the upregulation of miR-340 in circ_001680-overexpressing cells.	Downregulation	SW480, HCT116	Human	439
hsa-miR-328	MIMAT0000752	microRNA	22453125	2012	MicroRNA expression profiling identifies miR-328 regulates cancer stem cell-like SP cells in colorectal cancer	colorectal carcinoma (CRC)	The SP cells sorted from CRC possess cancer stem cell (CSC)-like properties, including self-renewal, differentiation, resistance to chemotherapy, invasive and strong tumour formation ability. MiR-328 expression was significantly reduced in SP cells compared with Non-SP cells. In addition, miR-328 overexpression reversed drug resistance and inhibited cell invasion of SP cells.	Downregulation	SW1116, LoVo, HCT116, SW480, SW620	Human	428
hsa-miR-328-3p	MIMAT0000752	microRNA	34045663	2022	Fatty acid beta-oxidation promotes breast cancer stemness and metastasis via the miRNA-328-3p-CPT1A pathway	breast cancer (BRCA)	MiR-328-3p was significantly downregulated in breast cancer, especially in patients with metastasis. The miR-328-3p or CPT1A or fatty acid beta-oxidation or stemness axis was shown responsible for breast cancer metastasis.	Downregulation	MCF-7, MDA-MB-468	Human	429
hsa-miR-328-3p	MIMAT0000752	microRNA	35669102	2022	MZF1 Transcriptionally Activated MicroRNA-328-3p Suppresses the Malignancy of Stomach Adenocarcinoma via Inhibiting CD44	stomach adenocarcinoma (STAD)	It was found that miR-328-3p was downregulated in STAD, and inhibition of miR-328-3p significantly promoted the growth, migration, invasion, and stemness of STAD cells, while miR-328-3p overexpression exerted reverse effects.	Downregulation	AGS, SNU16	Human	430
hsa-miR-342-3p	MIMAT0000753	microRNA	34842937	2022	MiR-342-3p inhibits LCSC oncogenicity and cell stemness through HDAC7 or PTEN axis	liver cancer (HULC)	MiR-342-3p inhibited LCSC oncogenicity and cell stemness by promoting PTEN and inhibiting HDAC7.	Downregulation	SMMC-7721	Human	440
hsa-miR-326	MIMAT0000756	microRNA	25173582	2015	Targeting the SMO oncogene by miR-326 inhibits glioma biological behaviors and stemness	glioma	MiR-326 overexpression decreased self-renewal and stemness and partially prompted differentiation in U251 tumor stem cells. The inhibition of Hh partially elevated miR-326 expression. Intracranial tumorigenicity induced by the transfection of miR-326 was reduced and was partially mediated by the decreased SMO expression.	Downregulation	U251	Human	426
hsa-miR-326	MIMAT0000756	microRNA	32511866	2020	CircRNA circ_POLA2 promotes lung cancer cell stemness via regulating the miR-326 or GNB1 axis	lung cancer (LC)	circ_POLA2 functioned as a ceRNA by sponging miR-326. Circ_POLA2 promotes lung cancer cell stemness and progression via regulating the miR-326 or GNB1 axis. Overexpression of miR-326 reduced the stemness of lung cancer cells, which was characterized as the decrease of sphere-formation capacity, ALDH1 activity, and stemness marker expression, which was rescued by GNB1 overexpression. The inhibitory effects of circ_POLA2 knockdown on the sphereformation ability were rescued by miR-326 inhibitor or GNB1 overexpression.	Downregulation	A549, H1651	Human	427
hsa-miR-151a-3p	MIMAT0000757	microRNA	34535770	2021	miR-151a-3p-rich small extracellular vesicles derived from gastric cancer accelerate liver metastasis via initiating a hepatic stemness-enhancing niche	gastric cancer (GC)	sEV-miR-151a-3p is highly expressed in GC-LM patients' plasma and presents poor prognosis. Furthermore, sEV-miR-151a-3p significantly accelerated the primary, secondary, and tertiary sphere formation of MKN45-LM cells. sEV-miR-151a-3p activates the TGF-beta1 SMAD2 or 3 pathway in hepatic metastatic GC cells via inhibiting SP3 in KCs, and thus promotes the proliferation, stem cell-like properties, and EMT of hepatic metastatic GC cells.	Upregulation	MKN45	Human	298
hsa-miR-135b	MIMAT0000758	microRNA	23623609	2013	miR-135b coordinates progression of ErbB2-driven mammary carcinomas through suppression of MID1 and MTCH2	breast cancer (BRCA)	MiR-135b silencing significantly reduced mammosphere generation in a sphere generation assay. MiR-135b silencing significantly reduced mammosphere generation in a sphere generation assay.	Upregulation	TUBO, TSA, 4T1	Human	254
hsa-miR-135b-5p	MIMAT0000758	microRNA	31510100	2019	Differentially Expressed microRNAs in MIA PaCa-2 and PANC-1 Pancreas Ductal Adenocarcinoma Cell Lines are Involved in Cancer Stem Cell Regulation	pancreatic ductal adenocarcinoma (PDAC)	We report the miRNA expression characteristics of two cell lines, MIA PaCa-2 and PANC-1, and discovered three miRNAs (miR-7-5p, let-7d, and miR-135b-5p) that are involved in cancer stem cells (CSCs) suppression. After transfection of each miRNA's mimic into PANC-1 cells which exhibits higher stemness feature than MIA-PaCa-3 cells, partial reduction of CSC surface markers and inhibition of tumor sphere formation were observed.	Downregulation	MIA PaCa-2, PANC-1	Human	256
hsa-miR-324-5p	MIMAT0000761	microRNA	34257080	2021	MicroRNA-324-5p-CUEDC2 Axis Mediates Gain-of-Function Mutant p53-Driven Cancer Stemness	non-small cell lung cancer (NSCLC)	MiR-324-5p is upregulated in human cancer cell lines and non-small cell lung carcinoma (NSCLC) tumors carrying TP53 GOF mutations. NF-kappaB due to downregulation of CUEDC2 by miR-324-5p imparts stemness in GOF mutant p53 cancer cells. We observed profound increase in miR-324-5p 379 expression in spheres as compared to their respective adherent counterparts, suggesting 380 enrichment of miR-324-5p in the stem cell populations. H1299 cells stably expressing miR-324-5p (H1299 or miR-324-5p) exhibited greater sphere forming ability, increased CD44Br and ALDHBr population as compared to empty vector carrying cells (H1299 or PLKO1). the increased sphere forming ability of H1299 or R273H cells was significantly 411 compromised upon miR-324-5p inhibition.	Upregulation	H1299, R273H	Human	425
hsa-miR-133b	MIMAT0000770	microRNA	31978895	2020	AR-induced ZEB1-AS1 represents poor prognosis in cholangiocarcinoma (CCA) and facilitates tumor stemness, proliferation and invasion through mediating miR-133b or HOXB9	cholangiocarcinoma (CCA)	Spheroid formation assay also suggested that silencing miR-133b partly rescued suppression of tumor stemness caused through knocking down ZEB1-AS1. Furthermore, tumor-promoting function generated through silencing miR-133b was saved by knocking down HOXB8 confirmed by the rescue assays of EdU, spheroid formation and transwell. Malignant phenotypes of CCA promoted by ZEB1-AS1 dysregulation were rescued separately through interfering miR-133b and HOXB8.	Downregulation	QBC939, CCLP-1	Human	251
hsa-miR-133b	MIMAT0000770	microRNA	31525340	2019	miR-133b suppresses colorectal cancer cell stemness and chemoresistance by targeting methyltransferase DOT1L	colorectal carcinoma (CRC)	Notably, the number of spheroids of HT29 and SW620 was dramatically decreased along with enforced miR-133b expression. MiR-133b is downregulated in colorectal spheroids, miR-133b overexpression reduces CRC stemness and overrides chemoresistance to 5-Fluorouracil (5-FU) and oxaliplatin (OXP).	Downregulation	HT29, SW620	Human	252
mmu-miR-215	MIMAT0000904	microRNA	28092415	2017	Cluster microRNAs miR-194 and miR-215 suppress the tumorigenicity of intestinal tumor organoids	intestinal tumors	MiR-194 and miR-215 was markedly suppressed in intestinal tumor organoids in comparison with organoids derived from normal intestinal epithelia. MiR-215 inhibits stemness of intestinal tumor organoids. Enforced expression of miR-215 suppressed the cancer stem cell signature through downregulation of intestinal stem cell markers including Lgr5.	Downregulation	Lgr5-positive stem cells	Mouse	379
hsa-miR-384	MIMAT0001075	microRNA	30819221	2019	Cross-talk among AFAP1-AS1, ACVR1 and microRNA-384 regulates the stemness of pancreatic cancer cells and tumorigenicity in nude mice	pancreatic cancer (PaCa)	There was no significant difference detected between miR-384 mimic-NC and miR-384 inhibitor-NC groups in terms of sphere number, sphere diameter, monoclonal formation rate, cell proliferation and invasion. However, comparing the two NC groups, the miR-384 mimic group exhibited a decreased sphere number, sphere diameter, monoclonal formation rate, cell proliferation and invasion, all of which were increased in the miR-384 inhibitor group. Therefore, inhibition of miR-384 enhances PC cell stemness.	Downregulation	PANC-1	Human	477
hsa-miR-196b-5p	MIMAT0001080	microRNA	28591704	2017	Maintenance of cancer stemness by miR-196b-5p contributes to chemoresistance of colorectal cancer cells via activating STAT3 signaling pathway	colorectal carcinoma (CRC)	MiR-196b-5p is dramatically upregulated in CRC tissues and high expression of miR-196b-5p correlates with poor survival in CRC patients. Silencing miR-196b-5p suppresses spheroids formation ability, the fraction of SP cells, expression of stem cell factors and the mitochondrial potential, and enhances the apoptosis induced by 5-fluorouracil in CRC cells. Downregulation of miR-196b-5p resensitizes CRC cells to 5-fluorouracil in vivo.	Upregulation	HCT116, SW480	Human	327
hsa-miR-424	MIMAT0001341	microRNA	26420065	2015	PBX3 is targeted by multiple miRNAs and is essential for liver tumour-initiating cells	hepatocellular carcinoma (HCC)	We used the TIC-enriched Hep-12 and the non-tumorigenic Hep-11 cell lines by genome-wide profiling of miRNA expression with miRNA microarray analysis, followed by functional screening with soft-agar assay and we got let-7c, miR-200b, miR-222 and miR-424 which resulted in a complete inhibition of tumour formation. The spheroid formation efficiency decreased significantly when the expression of the four miRNAs was induced individually by DOX.	Downregulation	Hep-12, Huh7	Human	482
hsa-miR-20b-5p	MIMAT0001413	microRNA	31012108	2019	Long noncoding RNA MALAT1 mediates stem cell-like properties in human colorectal cancer cells by regulating miR-20b-5p or Oct4 axis	colorectal carcinoma (CRC)	si-MALAT1 and miR-20b-5p-mimic attenuated microsphere formation and self-renewal capacity, decreased the proportion of CSCs, and downregulated the expression of proteins associated with tumor cell stemness maintenance (Oct4, Nanog, sex-determining region Y-box 2, and Notch1) and cellular metabolism (glucose transporter 1, lactate dehydrogenase B, hexokinase 2, and pyruvate kinase isozyme M2) in HCT-117 cells in vitro.	Downregulation	HCT-116	Human	365
hsa-miR-448	MIMAT0001532	microRNA	31232474	2019	microRNA-448 inhibits stemness maintenance and self-renewal of hepatocellular carcinoma stem cells through the MAGEA6-mediated AMPK signaling pathway	hepatocellular carcinoma (HCC)	MiR-448 activates the AMPK signaling pathway by downregulating MAGEA6, thus inhibiting the stemness maintenance and self-renewal of HCC stem cells.	Downregulation	Hep3B, L02	Human	489
hsa-miR-449a	MIMAT0001541	microRNA	28627667	2017	Loss of miR-449a-caused PrLZ overexpression promotes prostate cancer metastasis	prostate cancer (PCa)	MiR-449a expression was decreased in PCa cell lines. Moreover, miR-449a was downregulated in PCa tissues, especially in primary lesion tissues of metastatic PCa patients. Lentivirus mediated miR-449a overexpression suppressed proliferation of LNcap and PC-3, and miR-449a also significantly inhibited invasion and angiogenesis ability of LNcap and PC-3. Western blotting revealed that miR-449a overexpression and PrLZ shRNA all remarkably inhibited the stemness features in LNcap and PC-3.	Downregulation	PC-3, LNcap	Human	490
hsa-miR-450a-5p	MIMAT0001545	microRNA	32144236	2020	Regulation of cancer stem cell properties, angiogenesis, and vasculogenic mimicry by miR-450a-5p or SOX2 axis in colorectal cancer	colorectal carcinoma (CRC)	We also found that increased expression of miR-450a-5p significantly ceased CRC stemness including the sphere-forming capacity, CD133 expression. Knockdown of SOX2 ceased stemness properties, angiogenesis, and VM, along with decreased expression of CD133, CD31, and VE-cadherin as observed in functional experiments. MiR-450a-5p suppressed the expression of SOX2 by targeting its 3'UTR region directly and hence restrained SOX2-induced CSC properties, angiogenesis, and VM.	Downregulation	SW480, SW620	Human	491
hsa-miR-451a	MIMAT0001631	microRNA	34333815	2023	MiR-144 or 451a cluster synergistically modulates growth and metastasis of Oral Carcinoma	oral squamous cell carcinoma (OSCC)	MiR-144 and miR-451a were downregulated in all cell lines. However, UPCI-SCC029B showed a significant reduction in cell viability for miR-451a, miR-144 or 451a, and miR-144-5p transfected cells but not for miR-144-3p transfected cells. MiR-144 or 452a cluster functions as a tumor suppressor in OSCC by inhibiting cancer cell invasion, migration, and clonogenic potential.	Downregulation	UPCI-SCC029B, UM-SCC083A	Human	493
hsa-miR-452	MIMAT0001635	microRNA	23695168	2013	Downregulation of miR-452 promotes stem-like traits and tumorigenicity of gliomas	glioma	MiR-452 was markedly downregulated in glioma cells and clinical glioma tissues. MiR-452 directly targeted and suppressed multiple stemness regulators, including Bmi-1, LEF1, and TCF4, resulting in reduced stem-like traits and tumorigenesis of glioma cells in vitro and in vivo.	Downregulation	U87MG, LN-443	Human	495
hsa-miR-452	MIMAT0001635	microRNA	27058905	2016	MicroRNA-452 promotes stem-like cells of hepatocellular carcinoma by inhibiting Sox7 involving Wnt or beta-catenin signaling pathway	hepatocellular carcinoma (HCC)	MiR-452 was markedly increased in the chemo-resistant hepatospheres and human HCC tissues. MiR-452 significantly promoted stem-like characteristics in vitro and in vivo. Furthermore, tumor sphere assay showed that greater size and more hepatospheres were obtained in LM3 or miR-452 and Huh7 or miR-452 cells. Moreover, miR-452 down-regulation weakened the self-renewal ability of HCC cells presented with smaller size and less hepatospheres.	Upregulation	HCCLM3, Huh7	Human	496
hsa-miR-409-5p	MIMAT0001638	microRNA	24963047	2014	miR-409-3p or -5p promotes tumorigenesis, epithelial-to-mesenchymal transition, and bone metastasis of human prostate cancer	prostate cancer (PCa)	Ectopic expression of miR-409-3p or -5p in the prostate gland transforms normal prostate epithelia, promotes tumorigenicity, EMT, and stemness in vivo. We demonstrate that miR-409-3p or -5p is upregulated in two aggressive, bone metastatic EMT PCa models and in human embryonic stem cells and iPSCs. Human prostatic tissues with higher Gleason score and prostate cancer bone metastasis tissues express elevated levels of miR-409.	Upregulation	293T	Human	479
hsa-miR-409-3p	MIMAT0001639	microRNA	24963047	2014	miR-409-3p or -5p promotes tumorigenesis, epithelial-to-mesenchymal transition, and bone metastasis of human prostate cancer	prostate cancer (PCa)	Ectopic expression of miR-409-3p or -5p in the prostate gland transforms normal prostate epithelia, promotes tumorigenicity, EMT, and stemness in vivo. We demonstrate that miR-409-3p or -5p is upregulated in two aggressive, bone metastatic EMT PCa models and in human embryonic stem cells and iPSCs. Human prostatic tissues with higher Gleason score and prostate cancer bone metastasis tissues express elevated levels of miR-409.	Upregulation	293T	Human	478
hsa-miR-410	MIMAT0002171	microRNA	28076327	2017	MiR-410 induces stemness by inhibiting Gsk3beta but upregulating beta-catenin in non-small cells lung cancer	non-small cell lung cancer (NSCLC)	MiR-410 promotes stem cells-like properties such as proliferation, sphere formation, metastasis and chemoresistance. MiR-410 induces stemness through inhibiting Gsk3beta but increasing Sox2, Oct4, Nanog and CXCR4, which binds to beta-catenin signaling.	Upregulation	A549, H1299	Human	480
hsa-miR-484	MIMAT0002174	microRNA	32865695	2021	miR-484 suppresses endocrine therapy-resistant cells by inhibiting KLF4-induced cancer stem cells in estrogen receptor-positive cancers	breast cancer (BRCA)	In tamoxifen-resistant cells and breast CSCs, the expression of miR-484 was lower compared with that in parental cells. Overexpressing miR-484 in the breast and CSCs decreased the expression of stem cell molecular markers and sphere formation. MiR-484 plays a negative role in maintaining CSCs. Overexpressing miR-484 makes CSCs re-gained sensitization of tamoxifen. MiR-484 directly binds to KLF4 3-UTR and downregulates this activity.	Downregulation	MCF-7, T-47D	Human	501
hsa-miR-484	MIMAT0002174	microRNA	29480405	2018	miR-484 or MAP2 or c-Myc-positive regulatory loop in glioma promotes tumor-initiating properties through ERK1 or 2 signaling	glioma	MiR-484 enhanced glioma tumor-initiating properties in vitro and in vivo. Moreover, miR-484 was shown to directly target MAP2, resulting in activation of ERK1 or 2 signaling and promotion of stemness in glioma.	Upregulation	U87, U251	Human	502
hsa-miR-485-5p	MIMAT0002175	microRNA	36172827	2022	Circ_0001535 Facilitates Tumor Malignant Progression by miR-485-5p or LASP1 Axis in Colorectal Cancer	colorectal carcinoma (CRC)	Transwell assay and sphere formation showed that miR-485-5p mimics dampened cell invasion and stemness, whereas the effect was abrogated by elevating LASP1. MiR-485-5p inhibited the malignant behaviors of CRC cells by regulating LASP1 expression.	Downregulation	HCT116, LoVo, SW480, SW620	Human	504
hsa-miR-485-5p	MIMAT0002175	microRNA	35706019	2022	MicroRNA-485-5p targets keratin 17 to regulate oral cancer stemness and chemoresistance via the integrin or FAK or Src or ERK or beta-catenin pathway	oral squamous cell carcinoma (OSCC)	Ectopic expression of miRNA-485-5p inhibited OSCC sphere formation and caused sensitization of cancer cells towards cisplatin and carboplatin, which could be significantly rescued by KRT17 overexpression. A novel miRNA-485-5p or KRT17 or integrin or FAK or Src or ERK or beta-catenin signaling pathway is unveiled to modulate OSCC cancer stemness and drug resistance to the common first-line chemotherapeutics. The results demonstrated that miR-485-5p transfection significantly decreased the number of spheres formed, whereas KRT17 co-transfection rescued the inhibition of sphere formation by miR-485-5p in C9IV3 and HSC3 cells.	Downregulation	HSC3, C9IV3	Human	505
hsa-miR-486-5p	MIMAT0002177	microRNA	34323695	2021	The synergy between miR-486-5p and tamoxifen causes profound cell death of tamoxifen-resistant breast cancer cells	breast cancer (BRCA)	MiR-486-5p is significantly downregulated, whereas HMGA1 is considerably upregulated in ER+ BC samples. Combined treatment with miR-486-5p and tamoxifen also additively reduces cell migration, invasion, colony formation, mammary spheroid formation and a CD24-CD44+ cell population, representing decreased cancer stemness.	Downregulation	MCF-7	Human	506
hsa-miR-491-5p	MIMAT0002807	microRNA	33627127	2021	Long non-coding RNA VPS9D1-AS1 facilitates cell proliferation, migration and stemness in hepatocellular carcinoma	hepatocellular carcinoma (HCC)	Up-regulated SEC61A1 facilitated cell proliferation, migration and stemness in HCC cells. MiR-491-5p negatively regulated SEC61A1 and inhibited HCC cell proliferation and migration by targeting SEC61A2. Further, sphere formation assay and qRT-PCR detection of stemness biomarkers demonstrated that HCC cell stemness hindered by VPS9D1-AS1 silence was recovered by miR-491-5p down-regulation or SEC61A1 up-regulation.	Downregulation	HCCLM3, Huh-7	Human	509
hsa-miR-491-5p	MIMAT0002807	microRNA	34685504	2021	Identification of the Novel Tumor Suppressor Role of FOCAD or miR-491-5p to Inhibit Cancer Stemness, Drug Resistance and Metastasis via Regulating RABIF or MMP Signaling in Triple Negative Breast Cancer	triple negative breast cancer (TNBC)	MiR-491-5p targets RABIF by inhibiting its promotion of sphere formation, drug resistance, cell invasion, and pulmonary metastasis.	Downregulation	MDA-MB-231, Hs578T	Human	510
hsa-miR-146b-5p	MIMAT0002809	microRNA	27166258	2016	MiR-146b-5p overexpression attenuates stemness and radioresistance of glioma stem cells by targeting HuR or LINCRNA-p21 or beta-catenin pathway	glioblastoma (GBM)	MiR-146b-5p overexpression increased apoptosis and radiosensitivity, decreased cell viability, neurosphere formation capacity and stem cell marker expression, and induced differentiation in GSCs.	Downregulation	U87, SU-2	Human	289
hsa-miR-492	MIMAT0002812	microRNA	32065219	2020	miR-492 promotes chemoresistance to CDDP and metastasis by targeting inhibiting DNMT3B and induces stemness in gastric cancer	gastric cancer (GC)	MiR-492 overexpression in GC specimens and cell lines. The inhibition of miR-492 suppressed GC cell invasion and enhanced the sensitivity of gastric cancer cells to CDDP treatment. The inhibition of miR-492 stimulates GC stemness. MiR-492 exerts its anticancer role by targeting DNMT3B in GC.	Upregulation	SGC7901, AGS	Human	511
hsa-miR-494	MIMAT0002816	microRNA	26090866	2015	Activation of microRNA-494-targeting Bmi1 and ADAM10 by silibinin ablates cancer stemness and predicts favourable prognostic value in head and neck squamous cell carcinomas	head and neck squamous-cell carcinoma (HNSCC)	Quantitative RT-PCR analysis to confirm that miR-494 levels were low in ALDH1+ or CD44+ and sphere-forming HNC-TICs but high in ALDH1+ or CD44+ and parental cells. Overexpressed miR-494 decreased sphere-forming ability, side population, as well as the invasion ability in HNC-TICs. Silencing of endogenous miR-494 induced self-renewal capability in CD44+ or ALDH1+ cells.	Downregulation	S-G, SAS, OECM-1	Human	513
hsa-miR-494-3p	MIMAT0002816	microRNA	33594251	2021	Macrophage-derived EDA-A2 inhibits intestinal stem cells by targeting miR-494 or EDA2R or beta-catenin signaling in mice	inflammatory bowel disease (IBD)	MiR-494-3p-targeted EDA2R and the ligand EDA-A2, suppressed colonic stemness and epithelial repair by inhibiting beta-catenin or c-Myc.	Downregulation	EDA-A2	Human	514
hsa-miR-497-5p	MIMAT0002820	microRNA	34732693	2021	miR-497-5p or SALL4 axis promotes stemness phenotype of choriocarcinoma and forms a feedback loop with DNMT-mediated epigenetic regulation	choriocarcinoma	Silencing miR-497-5p and SALL4 promotes choriocarcinoma progression and forms a feedback loop with DNMT-mediated epigenetic regulation, playing a crucial role in stemness maintenance in choriocarcinoma.	Upregulation	JEG-3	Human	515
hsa-miR-515-5p	MIMAT0002826	microRNA	34774083	2021	Circular RNA circPIP5K1A contributes to cancer stemness of osteosarcoma by miR-515-5p or YAP axis	osteosarcoma (OS)	Next, we confirmed that the treatment of miR-515-5p mimic attenuated the sphere formation abilities of MG63 and 143B cells. We found that the depletion of circPIP5K1A or miR-515-5p mimic could attenuate the sphere formation abilities of MG63 and 143B cells, and the inhibition of miR-515-5p or YAP overexpression could rescue the attenuation effect of circPIP5K1A MG63 and 143B cells.	Upregulation	MG63, 143B	Human	523
hsa-miR-520b	MIMAT0002843	microRNA	28515423	2017	MiR-520b as a novel molecular target for suppressing stemness phenotype of head-neck cancer by inhibiting CD44	head and neck cancer (HNC)	MiR-520b inhibits the malignancy of HNC through regulation of cancer stemness conversion by targeting CD44. MiR-520b suppressed spheroid cell formation, as well as reduced expressions of multiple stemness regulators (Nestin, Twist, Nanog, Oct4). Administration of miR-520b dramatically restrained tumorigenesis and liver colonization.	Downregulation	OECM1, SAS	Human	526
hsa-miR-520c-3p	MIMAT0002846	microRNA	32633423	2021	An integrated analysis to predict micro-RNAs targeting both stemness and metastasis in human gastric cancer	gastric cancer (GC)	miR-200c-3p and miR-520c-3p overexpressed in MKN-45 gastrospheres and grade III tumors. miR-200c-3p and miR-520c-3p indicated a positive correlation with OCT4 and NOTCH1 expression in grade III tumors and MKN-46 spheres.	Upregulation	MKN-46	Human	527
hsa-miR-527	MIMAT0002862	microRNA	34433810	2021	hsa_circ_0003222 accelerates stemness and progression of non-small cell lung cancer by sponging miR-528	non-small cell lung cancer (NSCLC)	In contrast to hsa_circ_0003222, miR-527 expression levels were lower in tumor tissue. The suppressive result of hsa_circ_0003222 abolishing on NSCLC cell proliferation and stemness can be reversed to some extent by inhibiting miR-527.	Downregulation	PC9, A549	Human	528
hsa-miR-500a-3p	MIMAT0002871	microRNA	32588541	2020	Exosomal MiR-500a-3p promotes cisplatin resistance and stemness via negatively regulating FBXW7 in gastric cancer	gastric cancer (GC)	MiR-500a-3p was highly expressed in cisplatin (DDP) resistant GC cells (MGC803 or DDP and MKN45 or DDP) and their secreted exosomes than that in the corresponding parental cells. MGC803 or DDP-derived exosomes enhance DDP resistance and stemness properties of MGC803 recipient cells via exosomal delivery of miR-500a-3p in vitro and in vivo through targeting FBXW7.	Upregulation	MGC803, MKN45	Human	516
hsa-miR-500a-3p	MIMAT0002871	microRNA	28750679	2017	miR-500a-3p promotes cancer stem cells properties via STAT3 pathway in human hepatocellular carcinoma	hepatocellular carcinoma (HCC)	MiR-500a-3p is dramatically elevated in HCC tissues and cells and high expression of miR-500a-3p correlates with poor overall and relapse-free survival in HCC patients. Upregulating miR-500a-3p enhances, while silencing miR-500a-3p suppresses, the spheroid formation ability, fraction of side population and expression of cancer stem cell factors in vitro and tumorigenicity in vivo in HCC cells.	Upregulation	HepG2, Huh7	Human	517
hsa-miR-504	MIMAT0002875	microRNA	31419987	2019	miR-504 suppresses mesenchymal phenotype of glioblastoma by directly targeting the FZD7-mediated Wnt-beta-catenin pathway	glioblastoma (GBM)	MiR-504 overexpression suppressed malignant behaviors of GBM cells, such as migration, invasion, EMT, and stemness activity. MiR-504 was a negative regulator of the Wnt-beta-catenin pathway by directly repressing FZD7 expression, and FZD7 overexpression reversed the EMT inhibition caused by miR-504. The sphere-forming assay was used to determine whether miR-504 regulates the self-renewal ability of GSCs, and the results indicated that overexpression of miR-504 in GSCs suppressed their tumor sphere formation capability, while the inhibition of miR-504 increased it.	Downregulation	U87, 1295	Human	518
hsa-miR-504	MIMAT0002875	microRNA	33093452	2020	miR-504 modulates the stemness and mesenchymal transition of glioma stem cells and their interaction with microglia via delivery by extracellular vesicles	glioma	MiR-504 was significantly downregulated in GSCs compared with NSCs, its expression was lower in GBM compared with normal brain specimens and further decreased in the mesenchymal glioma subtype. Overexpression of miR-504 in GSCs inhibited their self-renewal, migration and the expression of mesenchymal markers.	Downregulation	glioma stem cells	Human	519
hsa-miR-506	MIMAT0002878	microRNA	30980388	2019	DGCR5 promotes cancer stem cell-like properties of radioresistant laryngeal carcinoma cells by sponging miR-506 via Wnt pathway	human laryngeal carcinoma	DGCR5 was upregulated and microRNA-506 (miR-506) was downregulated in Hep-2R cells. Overexpression of miR-506 also suppressed the CSC-like traits and the radiosensitivity was increased significantly. DGCR5 inhibition could repress Wnt signaling activity by sponging miR-506.	Downregulation	Hep-2, Hep-2R	Human	520
hsa-miR-508	MIMAT0002880	microRNA	29374066	2018	miR-508 Defines the Stem-like or Mesenchymal Subtype in Colorectal Cancer	colorectal carcinoma (CRC)	Ectopic expression of miR-508 in colorectal cancer cells blunted epithelial-to-mesenchymal transition (EMT), stemness, migration, and invasive capacity in vitro and in vivo In clinical colorectal cancer specimens, expression of miR-508 negatively correlated with stemness and EMT-associated gene expression and positively correlated with patient survival.	Downregulation	HCT116	Human	521
hsa-miR-509	MIMAT0002881	microRNA	35756764	2021	miR-509 inhibits cancer stemness properties in oral carcinomas via directly targeting PlK1	oral squamous cell carcinoma (OSCC)	The expression of miR-509 was downregulated in the CSCs derived from oral cancer cells (SAS), and upregulation of miR-509 diminished the several CSCs features, including ALDH1 activity, self-renewal capacity, CD44 expression, migration, and colony-forming abilities.	Downregulation	SAS	Human	522
hsa-miR-493-3p	MIMAT0003161	microRNA	34989145	2022	Circ_0007385 regulates cell proliferation, apoptosis and stemness via targeting miR-493-3p or RAB22A axis in non-small cell lung cancer	non-small cell lung cancer (NSCLC)	The tumor sphere-formation assay showed that miR-493-3p inhibited cell stemness. Circ_0007385 could regulate the development of NSCLC by sponging miR-493-3p to regulate the expression of RAB22A.	Downregulation	A549, H1299	Human	512
hsa-miR-487b-3p	MIMAT0003180	microRNA	33125503	2020	MicroRNA-487b-3p inhibits osteosarcoma chemoresistance and metastasis by targeting ALDH1A3	osteosarcoma (OS)	The expression level of microRNA(miR)-487b-3p in OS specimens and cell lines was found to be decreased. The overexpression of miR-487b-3p significantly inhibited OS cell migration and enhanced the sensitivity of OS cells to doxorubicin treatment. The overexpression of miR-487b-3p suppresses OS stemness.	Downregulation	Saos2	Human	507
hsa-miR-551a	MIMAT0003214	microRNA	30703870	2019	The MicroRNA-551a or MEF2C Axis Regulates the Survival and Sphere Formation of Cancer Cells in Response to 5-Fluorouracil	hepatocellular carcinoma (HCC)	MiR-551a-expressing cells (Hep3B-lenti-miR-551a) were resistant to 5-FU-induced cell death, and after 5-FU treatment, and showed significant increases in cell viability, cell survival, and sphere formation.	Upregulation	Hep3B	Human	530
hsa-miR-577	MIMAT0003242	microRNA	30879950	2019	miR-577 Regulates TGF-beta Induced Cancer Progression through a SDPR-Modulated Positive-Feedback Loop with ERK-NF-kappaB in Gastric Cancer	gastric cancer (GC)	MiR-577 is significantly upregulated in gastric cancer. miR-577 promotes metastasis and chemoresistance by inducing EMT and stemness-like properties. TGF-beta promotes the expression of miR-577, and miR-577 participates TGF-beta-mediated cancer metastasis.	Upregulation	MGC803	Human	531
hsa-miR-584-5p	MIMAT0003249	microRNA	30382096	2018	MiR-584-5p potentiates vincristine and radiation response by inducing spindle defects and DNA damage in medulloblastoma	medulloblastoma	MiR-584-5p mediated its tumor suppressor and therapy-sensitizing effects by targeting HDAC1 and eIF4E3. MiR-584-5p overexpression or HDAC1 or eIF4E3 silencing inhibited medulloblastoma stem cell self-renewal without affecting neural stem cell growth. MiR-584-5p mimic-transfected MB cells formed significantly smaller and fewer spheres.	Downregulation	D556Med, D425Med, D485Med	Human	532
hsa-miR-590-5p	MIMAT0003258	microRNA	28121351	2017	MicroRNA miR-590-5p inhibits breast cancer cell stemness and metastasis by targeting SOX2	breast cancer (BRCA)	MiR-590-5p inhibited breast cancer cell stemness through targeting SOX2. ALDEFLUOR Assay showed that miR-590-5p significantly decreased breast cancer stem cells population. NOD or SCID nude mice experiments indicated that miR-590-5p significantly inhibited tumorigenicity of breast cancer cells.	Downregulation	MCF-7, ZR75-1	Human	535
hsa-miR-600	MIMAT0003268	microRNA	35501825	2022	miR-600 promotes ovarian cancer cells stemness, proliferation and metastasis via targeting KLF9	ovarian cancer (OC)	MiR-600 expression was significantly upregulated in ovarian cancer tissues and stem cells. Functional studies showed that miR-600 promoted ovarian cancer cell stemness, proliferation and metastasis. MiR-600 promotes ovarian cancer cell stemness, proliferation and metastasis via directly downregulating KLF9.	Upregulation	HO8910, A2780	Human	536
hsa-miR-612	MIMAT0003280	microRNA	24704424	2014	MiR-612 suppresses the stemness of liver cancer via Wnt or beta-catenin signaling	hepatocellular carcinoma (HCC)	Our present findings reveal that miR-612 is able to suppress the stemness of HCC by reducing the number and size of tumorspheres as well as clone formation in soft agar, and to relieve drug resistance to cisplatin and 5-fluorouracil. MiR-612 hampered the capacity of tumorigenesis in NOD or SCID mice and redistributed the tumor invasive frontier of miR-612-modulating cells.	Downregulation	HCCLM3, HepG2	Human	538
hsa-miR-612	MIMAT0003280	microRNA	27685621	2016	miR-612 suppresses stem cell-like property of hepatocellular carcinoma cells by modulating Sp1 or Nanog signaling	hepatocellular carcinoma (HCC)	MiR-612 has a suppressive role on HCC stemness via Sp1 or Nanog signaling pathway.	Downregulation	HCCLM3, HepG2	Human	539
hsa-miR-33b	MIMAT0003301	microRNA	25919570	2015	MicroRNA-33b Inhibits Breast Cancer Metastasis by Targeting HMGA2, SALL4 and Twist1	breast cancer (BRCA)	The ectopic expression of miR-33b in BT-549 and MDA-MB-231 cells decreased the size and number of mammospheres in primary, secondary and tertiary cultures. However, at the 10-, 50-, 100- and 1,000-cell levels, BT-549 or ctrl and MDA-MB-231 or ctrl cells formed more mammospheres than BT-549 or miR-33b and MDA-MB-231 or miR-33b cells. Compared with paired normal breast tissues, miR-33b expression is downregulated in breast tumor samples, miR-33b knockdown promotes the self-renewal, migration and invasion capabilities of noncancerous mammary epithelial cells by targeting HMGA2, SALL4 and Twist1.	Downregulation	MDA-MB-231, BT-549	Human	435
hsa-miR-33b	MIMAT0003301	microRNA	35579082	2022	CircPCBP2 promotes the stemness and chemoresistance of DLBCL via targeting miR-33a or b to disinhibit PD-L1	diffuse large B-cell lymphoma (DLBCL)	CircPCBP2 was upregulated in human DLBCL specimens and cultured DLBCL cells while miR-33a or b was reduced. Knockdown of circPCBP2 or miR-33a or b overexpression inhibited the stemness of DLBCL cells and promoted cancer cell apoptosis upon CHOP treatment. CircPCBP2 enhances DLBCL cell stemness but suppresses its sensitivity to CHOP via sponging miR-33a or b to disinhibit PD-L1 expression.	Downregulation	U2932, OCI-LY3, SU-DHL-3, NU-DUL-1	Human	436
hsa-miR-637	MIMAT0003307	microRNA	33085838	2021	CircRNA EPHB4 modulates stem properties and proliferation of gliomas via sponging miR-637 and up-regulating SOX10	glioma	CircEPHB4 up-regulated SOX10 and Nestin by directly sponging miR-637, thereby stimulating stemness, proliferation and glycolysis of glioma cells. In contrast to the phenotypes achieved by altering circEPHB4, elevating miR-637 level using miR-637 mimics inhibited neurosphere formation and down-regulated cell surface expression of CD133, as well as the expression of multiple stemness biomarkers, including Nestin, Oct4, Nanog, CD133 and CD44.	Downregulation	SHG-44, LN229	Human	541
hsa-miR-638	MIMAT0003308	microRNA	31410735	2020	miR-638 represses the stem cell characteristics of breast cancer cells by targeting E2F2	breast cancer (BRCA)	MiR-638 mimic signifcantly decreased mammosphere numbers formed by BCSCs versus to control mimic group, while the numbers of mammosphere were signifcantly increased after E2F2 levels increased by pcDNA-E2F2 and miR-638 mimic co-transfection compared with miR-638 mimic group. The miR-638 was down-regulated and E2F2 was increased in BCSCs. MiR-638 represses the characteristics and behaviors of BCSCs by targeting E2F2.	Downregulation	MCF-10A, MCF-10A	Human	542
hsa-miR-641	MIMAT0003311	microRNA	34288821	2021	Circular RNA circSETD3 hampers cell growth, migration, and stem cell properties in bladder cancer through sponging miR-641 to upregulate PTEN	bladder cancer (BLCA)	Mechanistically, circSETD3 sponged miR-641 to upregulate PTEN, resulting in the blockage of BLCA progression. Our findings indicated that circSETD3 acted as a vital tumor suppressor in BLCA via regulating the miR-641 or PTEN axis.	Upregulation	T24, UMUC3	Human	543
hsa-miR-643	MIMAT0003313	microRNA	34528144	2022	CircLPAR3 Acts as an Oncogene in Oral Squamous Cell Carcinoma Through Regulating the miR-643 or HMGB2 Network	oral squamous cell carcinoma (OSCC)	CircLPAR3 could sponge miR-643 to positive regulate HMGB2. The promotion efect of circLPAR3 silencing on the apoptosis rate and the inhibitory efect on cell migration, invasion and sphere percentage rate also could be abolished by the addition of anti-miR-643. MiR-643 overexpression had an inhibition effect on OSCC progression, and its inhibitor could reverse the negative regulation of circLPAR3 knockdown on OSCC progression. In addition, overexpressed HMGB2 also reversed the suppressive effect of circLPAR3 silencing on OSCC progression.	Downregulation	Cal-27, SCC9	Human	544
hsa-miR-663a	MIMAT0003326	microRNA	34424812	2021	Up-regulation of miR-663a inhibits the cancer stem cell-like properties of glioma via repressing the KDM2A-mediated TGF-beta or SMAD signaling pathway	glioma	The results showed that miR-663a was down-regulated in glioblastoma tissues and cells. miR-663a mimics or miR-663a inhibitors were transfected into U-251-MG and pGBMC1 cells. The spheres of the two cells were evaluated by the cell spheres assay, and the results revealed that the sphere ability of the cells in the miR-663a group was reduced compared with that in the NC group, while that in the miR-663a-in group was promoted. Up-regulating miR-663a reduced glioma progression by inhibiting the KDM2A-mediated TGF-beta or Smad pathway.	Downregulation	U-251-MG, pGBMC1	Human	547
hsa-miR-654-5p	MIMAT0003330	microRNA	35235236	2022	LncRNA CASC15 regulates breast cancer cell stemness via the miR-654-5p or MEF2D axis	breast cancer (BRCA)	Rescue experiments were used to validate the role of the CASC15 or miR-654-5p or MEF2D axis in the stemness of BCSCs. qRT-PCR revealed that CASC15 expression was directly proportional to that of MEF2D mRNA, whereas miR-654-5p inhibition abolished this effect. Inhibition of CASC15 expression downregulated the expression of OCT4, Nanog, and SOX2 in MCF-7 cells and the development of CD44+ CD24 CSCs. However, inhibition of miR-654-5p or MEF2D overexpression abolished these effects. Rescue experiments of sphere formation showed that suppression of CASC15 expression reduced the self-renewal capacity of BCSCs, whereas miR-654-5p inhibition or overexpression of MEF2D abolished this effect.	Upregulation	MCF-7	Human	545
hsa-miR-421	MIMAT0003339	microRNA	30587549	2019	Epigenetic Silencing of miRNA-338-5p and miRNA-421 Drives SPINK1-Positive Prostate Cancer	prostate cancer (PCa)	Ectopic expression of miRNA-338-5p or -421 in SPINK1-positive cells abrogates oncogenic properties including cell-cycle progression, stemness, and drug resistance, and shows reduced tumor burden and distant metastases in a mouse model. Further, to confirm if miRNAs overexpression lead to decrease in CSC-like properties, prostatosphere assay, a surrogate model for testing enhanced stem cell-like properties was performed, a significant decrease in the size and prostatosphere formation efficiency was observed in 22RV1-miR-338-5p or -421 cells. Further, prostatospheres formed by miRNAs-overexpressing cells exhibit a significant reduction in the expression of genes implicated in self-renewal and stemness.	Downregulation	22RV1	Human	481
hsa-miR-425-5p	MIMAT0003393	microRNA	31131448	2019	Long noncoding RNA LINC-PINT regulates laryngeal carcinoma cell stemness and chemoresistance through miR-425-5p or PTCH1 or SHH axis	laryngeal carcinoma (LC)	MiR-425-5p was found to be overexpressed in HEp-2 stemness- enriched spheres in comparison to parental cells. Expectedly, tumor sphere assays also showed that inhibition of miR-425-5p moderately reduced cell self-renewal. MiR-425-5p inhibition may reduce laryngeal carcinoma cell stemness and enhance chemosensitivity to cisplatin.	Upregulation	HEp-2	Human	483
hsa-miR-454	MIMAT0003885	microRNA	32598931	2020	Exosomal release of microRNA-454 by breast cancer cells sustains biological properties of cancer stem cells via the PRRT2 or Wnt axis in ovarian cancer	breast cancer (BRCA)	231-derived exosomes carrying miR-454 disrupted the Wnt pathway by targeting PRRT2, thereby promoting CSC stemness in vitro and OC cell growth in vivo.	Upregulation	SKOV3, CoC1	Human	497
hsa-miR-765	MIMAT0003945	microRNA	35648115	2022	TRG16, targeted by miR-765, inhibits breast cancer stem cell-like properties via regulating the NF-kappaB pathway	breast cancer (BRCA)	TRG16, negatively regulated by miR-765, may inhibit the BC progression through regulating BC stem cell-like properties and this inhibition may be mediated by the NF-kappaB pathway. In the present study, we proved that TRG16 overexpression decreased CD44-positive cells, mammosphere quantity, and the expression of cell stemness markers.	Upregulation	MDA-MB-231, MCF-7	Human	562
hsa-miR-675	MIMAT0004284	microRNA	32610610	2020	Enhancement of Breast Cancer Cell Aggressiveness by lncRNA H19 and its Mir-675 Derivative: Insight into Shared and Different Actions	breast cancer (BRCA)	On the other hand, MDA-MB-231 cells stably overexpressing miR-675 also formed more mammospheres. Similarly, the miR-675 mimic increased and the miR-675 inhibitor decreased the sphere-forming capacity of native MCF-7 and SUM159PT cells, indicating that miR-675 was also involved in the sphere-forming capacity of breast cancer cells. In vitro, H19 and miR-675 enhance the cell migration and invasion, as well as colony formation.MiR-675 simultaneously increases the expression of both epithelial and mesenchymal markers, suggesting the induction of a hybrid phenotype or mesenchymal-to-epithelial transition (MET).	Upregulation	MDA-MB-231, MCF-7	Human	550
hsa-miR-93-3p	MIMAT0004509	microRNA	29258605	2017	miR-105 or 93-3p promotes chemoresistance and circulating miR-105 or 93-3p acts as a diagnostic biomarker for triple negative breast cancer	triple negative breast cancer (TNBC)	Therefore, a mammosphere formation assay was used to investigate the effect of miR-105 and miR-93-3p on cancer stemness. Knockdown of miR-105 or 93-3p together significantly reduced sphere size and numbers in BT-549 cells, suggesting that elevated expression of miR-105 or 93-3p may enhance chemoresistance and metastasis in TNBC patients. MiR-105 or 93-3p activates Wnt or beta-catenin signaling by downregulating SFRP1 and thereby promotes stemness, chemoresistance, and metastasis in TNBC cells.	Upregulation	BT-549, HCC70	Human	572
hsa-miR-29b-1-5p	MIMAT0004514	microRNA	28423652	2017	Suppressive role exerted by microRNA-29b-1-5p in triple negative breast cancer through SPIN1 regulation	breast cancer (BRCA)	MiR-29b-1-5p was downregulated in human TNBC tissues and cell lines. MiR-29b-1-5p expression inversely correlated with mammosphere stemness potential, and miR-29b-1 ectopic overexpression decreased TNBC cell growth, self-renewal, migration, invasiveness and paclitaxel resistance repressing WNT or betacatenin and AKT signaling pathways and stemness regulators.	Downregulation	MDA-MB-231, BT-20	Human	412
hsa-miR-181a-2-3p	MIMAT0004558	microRNA	35076757	2022	Identification of microRNA expression profiles of CD44+ ovarian cancer stem cells	ovarian cancer (OC)	Inhibition of miR-181a2-3p enhanced the sphere formation of CD44+ ovarian CSCs. MiR-181a-2-3p negatively regulates the stem cell-like properties of CD44+ ovarian CSCs by targeting EGR1.	Downregulation	SKOV3, A2780	Human	316
hsa-miR-185-3p	MIMAT0004611	microRNA	33204001	2020	Long non-coding RNA FOXD3-AS1 silencing exerts tumor suppressive effects in nasopharyngeal carcinoma by downregulating FOXD3 expression via microRNA-185-3p upregulation	nasopharyngeal carcinoma (NPC)	FOXD3-AS1 and FOXD3 exhibited increased expression levels, while miR-185-3p exhibited diminished levels in NPC.FOXD3-AS1 knockdown repressed cell stemness, colony formation, viability, invasion, migration, and in vivo tumor growth, and accelerated cell apoptosisFOXD3 silencing or miR-185-3p overexpression reversed the effects of lncRNA FOXD3-AS2.	Downregulation	C666-1, HK-2	Human	319
hsa-miR-130b-5p	MIMAT0004680	microRNA	33295145	2021	Elevated microRNA-130b-5p or silenced ELK1 inhibits self-renewal ability, proliferation, migration, and invasion abilities, and promotes apoptosis of cervical cancer stem cells	cervical cancer (CC)	Decreased miR-130b-5p and elevated ELK1 existed in CC tissues of patients. Up-regulated miR-130b-5p decreased ELK1 expression in CC stem cells. Elevated miR-130b-5p or silenced ELK1 inhibited self-renewal ability and stemness, colony formation, proliferation, migration and invasion abilities, promoted apoptosis of CC stem cells, as well as decreased the weight and volume of tumor in nude mice.	Downregulation	HeLa	Human	247
hsa-miR-371-5p	MIMAT0004687	microRNA	25868860	2015	The SOX17 or miR-371-5p or SOX2 axis inhibits EMT, stem cell properties and metastasis in colorectal cancer	colorectal carcinoma (CRC)	MiR-371-5p was obviously down-regulated in primary CRC tissues compared with matched adjacent normal mucosa and correlated significantly with differentiation, tumor size, lymphatic and liver metastases. Over-expression of miR-371-5p decreased the ability of cells to develop into spheres, and vice versa. MiR-371-5p could attenuate proliferation, invasion in vitro and metastasis in vivo in CRC cells. It also suppressed EMT by regulating Wnt or beta-catenin signaling and strongly decreased the CRC stemness phenotypes.	Downregulation	Lovo, SW480, HCT116	Human	465
hsa-miR-330-5p	MIMAT0004693	microRNA	31511040	2019	circPTN sponges miR-145-5p or miR-330-5p to promote proliferation and stemness in glioma	glioma	After establishing a stable overexpression system of mimic miR-145-5p through the lentiviral transfection of G15 cells, we determined that the sphere percentage and the levels of Nestin, CD133, SOX2, and SOX9, as well as tumor sphere percentage were markedly decreased in the mimic miR-145-5p group compared with the NC group.	Upregulation	G15, U87-GSC, U251-GSC	Human	431
hsa-miR-338-5p	MIMAT0004701	microRNA	30225541	2018	MicroRNA-338-5p plays a tumor suppressor role in glioma through inhibition of the MAPK-signaling pathway by binding to FOXD1	glioma	Glioma tissues had decreased expression of miR-338-5p. Overexpression of miR-338-5p suppresses glioma cell proliferation, migration, and invasion and accelerates its senescence and apoptosis by decreasing FOXD1 expression via inhibition of activation of MAPK-signaling pathway.	Downregulation	U251	Human	432
hsa-miR-338-5p	MIMAT0004701	microRNA	30587549	2019	Epigenetic Silencing of miRNA-338-5p and miRNA-421 Drives SPINK1-Positive Prostate Cancer	prostate cancer (PCa)	Ectopic expression of miRNA-338-5p or -421 in SPINK1-positive cells abrogates oncogenic properties including cell-cycle progression, stemness, and drug resistance, and shows reduced tumor burden and distant metastases in a mouse model. Further, to confirm if miRNAs overexpression lead to decrease in CSC-like properties, prostatosphere assay, a surrogate model for testing enhanced stem cell-like properties was performed, a significant decrease in the size and prostatosphere formation efficiency was observed in 22RV1-miR-338-5p or -421 cells. Further, prostatospheres formed by miRNAs-overexpressing cells exhibit a significant reduction in the expression of genes implicated in self-renewal and stemness.	Downregulation	22RV1	Human	433
hsa-miR-490-5p	MIMAT0004764	microRNA	30206962	2019	MiR-490-5p inhibits the stemness of hepatocellular carcinoma cells by targeting ECT2	hepatocellular carcinoma (HCC)	MiR-490-5p was remarkably downregulated, yet ECT2 was upregulated in HCC tissues compared with adjacent tissues. Overexpression of miR-490-5p restrained the sphere formation ability, stemness, and proliferation of HCC cells. MiR-490-5p repressed the stemness of HCC cells through inhibiting the expression of ECT2.	Downregulation	HepG2	Human	508
hsa-miR-532-3p	MIMAT0004780	microRNA	33298070	2020	ETS1-activated SNHG10 exerts oncogenic functions in glioma via targeting miR-532-3p or FBXL19 axis	glioma	MiR-532-3p was validated to bind with SNHG10 and expressed at a low level in glioma cells. Additionally, ectopic expression of miR-532-3p caused a decline in sphere formation efficiency and in the levels of stemness-related markers. FBXL19 targeted by miR-532-3p facilitated cell growth and stemness in glioma, and that SNHG10 worked in glioma by increasing FBXL19 expression through sequestering miR-532-3p.	Downregulation	U138, U251	Human	529
hsa-miR-455-3p	MIMAT0004784	microRNA	28633632	2017	Antagonizing miR-455-3p inhibits chemoresistance and aggressiveness in esophageal squamous cell carcinoma	esophageal squamous cell carcinoma (ESCC)	MiR-455-3p expression was found to be significantly associated with stemness signatures, miR-455-3p-transduced cells formed larger and more numerous tumorspheres containing higher proportions of CD90+ or CD271+ and SP cells than control cells.	Upregulation	Eca109, Kyse30, EC-CR, EC-UT	Human	498
hsa-miR-589-5p	MIMAT0004799	microRNA	27835990	2016	miR-589-5p inhibits MAP3K8 and suppresses CD90+ cancer stem cells in hepatocellular carcinoma	hepatocellular carcinoma (HCC)	Overexpression of miR-589-5p suppressed CD90+ CSC characteristics such as Oct4, Sox2 and Nanog expression, a high likelihood of forming cell spheres, high invasiveness and high tumorigenicity.	Upregulation	MHCC97H, MHCC97L	Human	533
hsa-miR-589-5p	MIMAT0004799	microRNA	29196128	2018	Maintenance of stemness by miR-589-5p in hepatocellular carcinoma cells promotes chemoresistance via STAT3 signaling	hepatocellular carcinoma (HCC)	MiR-589-5p is elevated in HCC tissues. Upregulating miR-589-5p enhances spheroid formation ability, fraction of CD133 positive and side population cells, expression of cancer stem cell factors and the mitochondrial potential, and represses the apoptosis induced by doxorubicin in vitro and tumorigenicity in vivo in HCC cells. MiR-589-5p promotes the cancer stem cell characteristics and chemoresistance via targeting multiple negative regulators of STAT3 signaling pathway	Upregulation	HepG2, Huh-7	Human	534
hsa-miR-628-5p	MIMAT0004809	microRNA	35710817	2022	Leptin modulated microRNA-628-5p targets Jagged-1 and inhibits prostate cancer hallmarks	prostate cancer (PCa)	Enforced expression of miR-628 in PCa cells inhibited cell proliferation, reduced PCa cell survival or migration or invasion or spheroid formation, and decreased markers of cell stemness. Mechanistically, miR-628 binds with the JAG1-3'UTR and inhibits the expression of Jagged-1 (JAG1). JAG1 inhibition by miR-628 downregulated Notch signaling, decreased the expression of Snail or Slug, and modulated epithelial-mesenchymal transition and invasiveness in PC3 cells.	Downregulation	DU145, PC3, 22Rv1, MDA-PCa-2B	Human	540
hsa-miR-298	MIMAT0004901	microRNA	35188404	2022	sh-HNF1A-AS1 reduces the epithelial-mesenchymal transition and stemness of esophageal cancer cells	esophageal squamous cell carcinoma (ESCC)	Furthermore, miR-298 inhibitor strongly increased the sphere diameter, which could be reversed by sh-HNF1A-AS1. The diameter of a sphere in the sh-HNF1A-AS1+miR-298 inhibitor group was much smaller than that in the miR-298 inhibitor group. Knockdown of HNF1A-AS1 could inhibit EMT and stemness by regulating the miR-298 or TCF4 axis.	Downregulation	EC109, KYSE-70	Human	407
hsa-miR-450b-5p	MIMAT0004909	microRNA	26845645	2016	miR-450b-5p Suppresses Stemness and the Development of Chemoresistance by Targeting SOX2 in Colorectal Cancer	colorectal carcinoma (CRC)	We demonstrated that expression of miR-450b-5p was downregulated in recurrent CRC tissues. Expression of miR-450b-5p was negatively correlated to the expression of SOX2, the percentages of CD133+ cells present, and sphere-forming capacity in CRC cells.	Downregulation	HT-29, HCT-116	Human	492
hsa-miR-876-5p	MIMAT0004924	microRNA	33619796	2021	CircVAPA exerts oncogenic property in non-small cell lung cancer by the miR-876-5p or WNT5A axis	non-small cell lung cancer (NSCLC)	CircVAPA acted as a competing endogenous RNA to up-regulate WNT5A by sponging miR-876-5p. Moreover, circVAPA activated Wnt or beta-catenin signaling by up-regulation of WNT5A. Rescue assays showed that silencing of miR-876-5p or overexpression of WNT5A reversed the circVAPA knockdown-mediated inhibition on cellular processes in NSCLC. Moreover, miR-876-5p inhibition or WNT5A upregulation reversed the inhibitory functions of circVAPA depletion on cell stemness maintenance.	Downregulation	H1299, H1975	Human	564
hsa-miR-708-5p	MIMAT0004926	microRNA	31468594	2019	LncRNA LOXL1-AS1 facilitates the tumorigenesis and stemness of gastric carcinoma via regulation of miR-708-5p or USF1 pathway	gastric cancer (GC)	LOXL1-AS1 acted as a ceRNA to upregulate USF1 via sponging miR-708-5p. Furthermore, we observed that the heightened sphere-forming ability induced by downregulation of miR-708-5p was repressed by USF1 depletion. Rescue experiments testified the stimulative role of LOXL1-AS1 or miR-708-5p or USF1 pathway in gastric cancer progression.	Downregulation	MKN-45, AGS	Human	555
hsa-miR-708-5p	MIMAT0004926	microRNA	28972040	2018	Downregulation of DNMT3A by miR-708-5p Inhibits Lung Cancer Stem Cell-like Phenotypes through Repressing Wnt or beta-catenin Signaling	lung cancer (LC)	MiR-708-5p suppresses NSCLC initiation, development, and stemness through interfering DNMT3A-dependent DNA methylation. MiR-708-5p decreased tumor sphere formation.	Downregulation	A549, Calu-3, 95D	Human	556
hsa-miR-744	MIMAT0004945	microRNA	26485754	2015	MiR-744 increases tumorigenicity of pancreatic cancer by activating Wnt or beta-catenin pathway	pancreatic cancer (PaCa)	We found that miR-744 was significantly upregulated in tumor tissues compared to normal tissues. A tumor sphere formation assay showed that miR-744-transduced cells formed a larger number of spheres with increased diameter compared to vector control cells. Upregulation of miR-744 promotes CSC-like traits and tumorigenicity in pancreatic cancer cells.	Upregulation	AsPC-1, MIA PaCa-2	Human	559
hsa-miR-665	MIMAT0004952	microRNA	34175686	2021	Circ_0030586 inhibits cell proliferation and stemness in bladder cancer by inactivating the ERK signaling via miR-665 or NR4A3 axis	bladder cancer (BLCA)	MiR-665 exhibited high expression in BCa tissues and cells while NR4A3 expression was downregulated in BCa. MiR-665 overexpression or NR4A3 silencing reversed the suppressive effect of circ_0030586 overexpression on BCa cell proliferation and stemness.	Upregulation	UMUC3, 5637	Human	549
hsa-miR-873	MIMAT0004953	microRNA	30803931	2019	MiR-873 or PD-L1 axis regulates the stemness of breast cancer cells	breast cancer (BRCA)	MiR-873 inhibited PD-L1 expression through directly binding to its 3'-untranslated region (UTR), and miR-873 attenuated the stemness and chemoresistance of breast cancer cells which was dependent on PD-L1 and the downstream PI3K or Akt and ERK1 or 2 signaling.	Downregulation	MCF-7, MDA-MB-231	Human	563
hsa-miR-1181	MIMAT0005826	microRNA	25444909	2015	MiR-1181 inhibits stem cell-like phenotypes and suppresses SOX2 and STAT3 in human pancreatic cancer	pancreatic cancer (PaCa)	We reported in pancreatic cancer tissues and cells that miR-1181 expression was markedly downregulated,overexpression of miR-1181 inhibited, whereas downregulation of miR-1181 promoted, CSCs-like phenotypes in vitro and tumorigenicity in vivo in pancreatic cancer cells. MiR-1181 upregulation dramatically decreased, while anti-miR-1181 increased, the sphere formation ratio of AsPC-1 and PANC-1 cells.	Downregulation	AsPC-1, PANC-1	Human	221
hsa-miR-663b	MIMAT0005867	microRNA	31758392	2020	miR-663b promotes colorectal cancer progression by activating Ras or Raf signaling through downregulation of TNK1	colorectal carcinoma (CRC)	MiR-663b was significantly overexpressed in colorectal tumors and cell lines. Downregulation of miR-663b inhibited cell proliferation and sphere forming ability in colorectal cancer cells. In addition, miR-663b downregulation inactivated Ras or Raf signaling activity and subsequently decreased YAP1 and CD44 expression in colorectal cancer cells.	Upregulation	HCT116, HT29	Human	548
hsa-miR-1290	MIMAT0005880	microRNA	26711929	2016	Hsa-miR-1246 and hsa-miR-1290 are associated with stemness and invasiveness of non-small cell lung cancer	non-small cell lung cancer (NSCLC)	Expressions of miR-1246 and miR-1290 on the 9th day of culture were increased proportionally to completeness of sphere-formation. Sphere-forming assay showed that there were significant suppressive effects of anti-miR-1246 andanti-miR-1290 onsphereformation of A549 and HCC1588. The number and size of sphere were significantly reduced by inhibition of miR-1246 and miR-1290. The effect of anti-miR-1290 on sphere-formation was stronger than that of anti-miR-1246 in A549. Anti-miR-1246 and anti-miR-1290 suppressed both the 1st and 2nd sphere formation in A549 and HCC1588. Anti-miR-1246 and anti-miR-1291 suppressed proliferation, sphere-formation, colony formation and invasion of NSCLC.	Upregulation	A549, HCC1588	Human	241
hsa-miR-1290	MIMAT0005880	microRNA	35220610	2022	Hsa-miR-1290 is associated with stemness and invasiveness in prostate cancer cell lines by targeting RORA	prostate cancer (PCa)	MiR-1290 showed overexpression within PC cells and tissues. According to our results, cells with inhibited miR-1290 expression formed a smaller number of spheres in low attachment growth condition. Moreover, as revealed by Transwell invasion and migration assays, miR-1290 silencing remarkably suppressed cell invasion and migration of the above-mentioned cells. We also collected the spheres and examined the expression patterns of stem cell markers including CD133, Oct4, Sox2, Nanog, c-Kit and Notch3. MiR-1290 up-regulation enhances PC cell growth and invasion by regulating RORA expression.	Upregulation	LNCaP, PC-3	Human	242
hsa-miR-1291	MIMAT0005881	microRNA	34981812	2022	Functional assessment of miR-1291 in colon cancer (CC) cells	colorectal carcinoma (CRC)	It was identified that miR-1291 significantly suppressed the proliferation, invasion, cell mobility and colony formation of CRC cells. Furthermore, miR-1291 suppressed cancer stem cell markers BMI1 and CD133, and inhibited sphere formation.	Downregulation	HCT116	Human	243
hsa-miR-1245a	MIMAT0005897	microRNA	35081869	2022	Hsa_circ_0006677 regulates special AT-rich binding protein-2-mediated tumor-suppressive effect via functioning as a miR-1245a sponge in non-small cell lung cancer	non-small cell lung cancer (NSCLC)	Circ_0006677 functioned as a miR-1245a sponge and mediated SATB2 expression through adsorbing miR-1245a. Either miR-1245a overexpression or SATB2 knockdown weakened circ_0006677 overexpression-mediated repression on proliferation, invasion, migration, and stemness.	Upregulation	H1299, A549	Human	227
hsa-miR-1246	MIMAT0005898	microRNA	27639189	2016	Octamer 4 or microRNA-1246 signaling axis drives Wnt or beta-catenin activation in liver cancer stem cells	liver cancer (HULC)	MiR-1246 promotes cancer stemness, including self-renewal, drug resistance, tumorigencity, and metastasis, by activation of the Wnt or beta-catenin pathway through suppressing the expression of AXIN2 and glycogen synthase kinase 3beta (GSK3beta), two key members of the beta-catenin destruction complex.	Upregulation	Huh7	Human	228
hsa-miR-1246	MIMAT0005898	microRNA	35894553	2022	MiR-1246 is responsible for lung cancer cells-derived exosomes-mediated promoting effects on lung cancer stemness via targeting TRIM17	lung cancer (LC)	It was found that miR-1246 was remarkably enriched in cisplatin-resistant lung cancer cells or exosomes and spheres. Inhibition of miR-1246 attenuated the stemness of lung cancer cells induced by exosomes from cisplatin-resistant cells and spheres.	Upregulation	HEK293T, A549	Human	229
hsa-miR-1246	MIMAT0005898	microRNA	26711929	2016	Hsa-miR-1246 and hsa-miR-1290 are associated with stemness and invasiveness of non-small cell lung cancer	non-small cell lung cancer (NSCLC)	Expressions of miR-1246 and miR-1290 on the 9th day of culture were increased proportionally to completeness of sphere-formation. Sphere-forming assay showed that there were significant suppressive effects of anti-miR-1246 andanti-miR-1290 onsphereformation of A549 and HCC1588. The number and size of sphere were significantly reduced by inhibition of miR-1246 and miR-1290. The effect of anti-miR-1290 on sphere-formation was stronger than that of anti-miR-1246 in A549. Anti-miR-1246 and anti-miR-1290 suppressed both the 1st and 2nd sphere formation in A549 and HCC1588. Anti-miR-1246 and anti-miR-1291 suppressed proliferation, sphere-formation, colony formation and invasion of NSCLC.	Upregulation	A549, HCC1588	Human	230
hsa-miR-1246	MIMAT0005898	microRNA	25117811	2014	MicroRNA-1246 expression associated with CCNG2-mediated chemoresistance and stemness in pancreatic cancer	pancreatic cancer (PaCa)	Outstanding expression of miR-1246 revealed by miRNA microarray analysis,the miR-1246 OE (Sp) enriched by sphere assay revealed that the proliferation rate was higher than control cells. The miR-1246 OE sphere increased significantly compared to control.	Upregulation	Panc1	Human	231
hsa-miR-1253	MIMAT0005904	microRNA	34620741	2022	Exosomal circ_0007385 enhances non-small cell lung cancer cell proliferation and stemness via regulating miR-1253 or FAM83A axis	non-small cell lung cancer (NSCLC)	MiR-1253 was a direct target of circ_0007385, and miR-1253 reversed the inhibitory effects of circ_0007385 on cell proliferation and stemness in NSCLC cells miR-1253 inhibition counteracted the inhibitory effects of circ_0007385 silencing on sphere formation efficiency and the protein levels of OCT4 and NANOG. Moreover, FAM83A was a direct target of miR-1253, and miR-1253 suppressed NSCLC cell proliferation and stemness by targeting FAM83A.	Downregulation	A549, H1299	Human	234
hsa-miR-1258	MIMAT0005909	microRNA	27270326	2016	Loss of miR-1258 contributes to carcinogenesis and progression of liver cancer through targeting CDC28 protein kinase regulatory subunit 1B	hepatocellular carcinoma (HCC)	Stable overexpression of miR-1258 suppresses cell migration, stemness and increases sensitivity of HCC cells to chemotherapy drug like doxorubicin.	Downregulation	HuH7, HCCLM3	Human	235
hsa-miR-1275	MIMAT0005929	microRNA	32194819	2020	HIF-1alpha-regulated miR-1275 maintains stem cell-like phenotypes and promotes the progression of LUAD by simultaneously activating Wnt or beta-catenin and Notch signaling	lung adenocarcinoma (LUAD)	MiR-1275 was highly upregulated in lung cancer cell lines and LUAD tissues. The number of spheres increased by approximately 40-50percentage in the miR-1275-upregulated LUAD cells but decreased in miR-1275-silenced LUAD cells. Furthermore, miR-1275 inhibitor reversed miR-1275-mediated sphere formation. MiR-1275 as a potential oncogene in LUAD that exerts its tumorigenic effect through co-activating Wnt or beta-catenin and Notch signaling pathways.	Upregulation	A549, PC9, H1299	Human	239
hsa-miR-1322	MIMAT0005953	microRNA	35569812	2022	Circ_0000291 contributes to hepatocellular carcinoma tumorigenesis by binding to miR-1322 to up-regulate UBE2T	hepatocellular carcinoma (HCC)	Circ_0000291 directly interacted with miR-1322 and negatively regulated miR-1322 expression. Circ_0000291 knockdown-mediated anti-tumor impacts in HCC cells were largely overturned by the interference of miR-1322.Circ_0000291 positively regulated UBE2T expression by absorbing miR-1322 in HCC cells.	Downregulation	Huh-7, LM6	Human	248
hsa-miR-1322	MIMAT0005953	microRNA	35569812	2022	Circ_0000291 contributes to hepatocellular carcinoma tumorigenesis by binding to miR-1322 to up-regulate UBE2T	hepatocellular carcinoma (HCC)	Circ_0000291 silencing suppressed the stemness of HCC cells, which was largely rescued by the introduction of anti-miR-1322. Additionally, circ_0000291 knockdown reduced the protein levels of PCNA, Slug, and SOX2 and increased the protein expression of Bax, and these effects were largely reversed by miR-1322 knockdown. These data revealed that circ_0000291 silencing suppressed HCC progression largely by up-regulating miR-1322 in vitro.	Downregulation	Huh-7, LM6	Human	249
hsa-miR-711	MIMAT0012734	microRNA	35786646	2022	MiR-711 regulates gastric cancer progression by targeting CD44	gastric cancer (GC)	In GC tissues and cell lines, the expression of miR-711 was down-regulated when compare with adjacent tissues or normal epithelial cells. The results indicated that overexpressing of miR-711 could suppress the GC cell proliferation, migration, and invasion through targeting CD44.	Downregulation	NCI-N87, SUN-1	Human	557
hsa-miR-2861	MIMAT0013802	microRNA	29620443	2018	MiR-2861 Behaves as a Biomarker of Lung Cancer Stem Cells and Regulates the HDAC5-ERK System Genes	lung cancer (LC)	MiR-2861 expression was significantly higher in LCSCs no matter compared to the differentiation cells or normal cells. HDAC5 expression was positively correlated with miR-2861 in LCSCs, and knockdown of miR-2861 decreased the expression of HDAC5, which implied that HDAC5 may be involved in the differentiation of LCSCs mediated by miR-2861.	Upregulation	H460, H1299	Human	404
hsa-miR-3065-3p	MIMAT0015378	microRNA	34656128	2021	miR-3065-3p promotes stemness and metastasis by targeting CRLF1 in colorectal cancer	colorectal carcinoma (CRC)	MiR-3065-3p was overexpressed in colorectal cancer and that its high expression was associated with poor prognosis of patients with colorectal cancer. Ectopic miR-3065-3p expression also promoted the sphere formation ability of CRC cells. MiR-3065-3p promoted the stemness and metastasis of colorectal cancer by targeting CRLF1.	Upregulation	HCT116, RKO	Human	419
hsa-miR-4319	MIMAT0016870	microRNA	31853229	2019	MiR-4319 induced an inhibition of epithelial-mesenchymal transition and prevented cancer stemness of HCC through targeting FOXQ1	hepatocellular carcinoma (HCC)	The level of miR-4319 was remarkably decreased in HCC specimens and cells compared to that in normal counterparts. miR-4319 repressed cell proliferation, accelerated apoptosis, inhibited EMT and prevented cancer stemness in HCC cells by targeting FOXQ1. An in vivo tumourigenesis assay uncovered that depletion of miR-4319 in Hep3B cells increased tumour growth and elevated the expression of EMT and CSC markers in comparison to those of the control group.	Downregulation	Hep3B, MHCC-97H	Human	485
hsa-miR-4319	MIMAT0016870	microRNA	30021199	2018	MiR-4319 Suppress the Malignancy of Triple-Negative Breast Cancer by Regulating Self-Renewal and Tumorigenesis of Stem Cells	triple negative breast cancer (TNBC)	MiR-4319 has differential expression between TNBC and non-TNBC stem cells. MiR-4319 could suppress the self-renewal and formation of tumorspheres in TNBC CSCs through E2F2, and also inhibited tumor initiation and metastasis in vivo.	Downregulation	MDA-MB-468, MDA-MB-231, MDA-MB-453	Human	486
hsa-miR-4262	MIMAT0016894	microRNA	35698305	2022	Hsa_circ_0001550 facilitates colorectal cancer progression through mediating microRNA-4262 or nuclear casein kinase and cyclin-dependent kinase substrate 1 cascade	colorectal carcinoma (CRC)	CRC cell stemness regulated by sh-hsa_circ_0001550 was rescued by miR-4262 interference. Hsa_circ_0001550 targeted miR-4262, and hsa_circ_0001550 absence-caused impacts were diminished by anti-miR-4262. MiR-4262 targeted NUCKS1. Hsa_circ_0001550 had positive regulation on NUCKS1 expression. NUCKS1 overexpression overturned the influences of hsa_circ_0001550 silencingon CRC cell progression.	Downregulation	SW480, HCT116	Human	484
hsa-miR-378d	MIMAT0018926	microRNA	33823894	2021	Chemotherapy-elicited exosomal miR-378a-3p and miR-378d promote breast cancer stemness and chemoresistance via the activation of EZH2 or STAT3 signaling	breast cancer (BRCA)	To investigate the function of exosome-derived miR-378a-3p and miR-378d, CAL51 and MDA-MB-231 cells were transfected with miR-378a-3p and miR-378d mimics or negative control (NC), and post-transfection cells were subjected to drug sensitivity assays, CD44+ or CD24- population analyses and sphere formation assays. MiR-378a-3p and miR-378d were found to contribute to the decreased drug sensitivity of cells to DOX and PTX and increased percentage of cancer stem cells. Similar results were obtained with MCF7 cells. Chemotherapy-elicited exosomal miR-378a-3p and miR-378d regulate the WNT or beta-catenin and Notch stemness pathways by targeting NUMB and DKK3.	Upregulation	CAL51, MDA-MB-231, MCF-7	Human	475
hsa-miR-378e	MIMAT0018927	microRNA	28121625	2017	Cancer-associated fibroblasts release exosomal microRNAs that dictate an aggressive phenotype in breast cancer	breast cancer (BRCA)	Differential expression profile analysis identified three miRs (miRs -21, -378e, and -143) increased in exosomes from CAFs as compared from normal fibroblasts. Normal fibroblast exosomes transfected with miRs -21, -378e, and -145 promoted the stemness and EMT phenotype of breast cancer cells.	Upregulation	T47D, BT549, MDA-MB-231	Human	476
hsa-miR-4428	MIMAT0018943	microRNA	35599309	2022	LINC01806 mediated by STAT1 promotes cell proliferation, migration, invasion, and stemness in non-small cell lung cancer through Notch signaling by miR-4428 or NOTCH2 axis	non-small cell lung cancer (NSCLC)	Likewise, we observed that the attenuated sphere-forming ability of NSCLC cells caused by LINC01806 depletion was enhanced upon miR-4428 down-regulation or NOTCH2 overexpression. LINC01806 knockdown impeded cell proliferation, migration, invasion, and stemness, along with tumor growth. LINC01806 enhanced NOTCH2 expression to stimulate Notch signaling via sponging miR-4428, thereby facilitating NSCLC progression.	Downregulation	H1650, H1299	Human	487
hsa-miR-4466	MIMAT0018993	microRNA	35461327	2022	Exosomal miR-4466 from nicotine-activated neutrophils promotes tumor cell stemness and metabolism in lung cancer metastasis	lung cancer (LC)	Tumorsphere and colony formation in miR-4466 transduced H2030BrM cells that showed a significant increase in CSC, tumorsphere and tumor cells growth relative to control cells. Exosomal miR-4466 levels were found to be elevated in serum or urine of cancer-free subjects with a smoking history and promote tumor growth in vivo.	Upregulation	H2030BrM	Human	488
hsa-miR-3120-5p	MIMAT0019198	microRNA	29307822	2018	miR-3120-5p promotes colon cancer (CC) stem cell stemness and invasiveness through targeting Axin2	colon cancer (CC)	MiR-3120-5p promotes stemness and invasiveness of colon cancer (CC) cells through direct targeting of Axin2.	Upregulation	HCT-116,SW-480	Human	423
hsa-miR-4711-5p	MIMAT0019816	microRNA	32066912	2020	miR-4711-5p regulates cancer stemness and cell cycle progression via KLF5, MDM2 and TFDP1 in colon cancer (CC) cells	colon cancer (CC)	MiR-4711-5p suppressed cell proliferation, migration and invasion ability, as well as stemness, including decreased stem cell marker expression, reactive oxygen species activity and sphere formation ability. MiR-4711-5p to MDM2 could upregulate wild-type p53, leading to strong induction of apoptosis.	Downregulation	DLD-1, HCT116	Human	499
hsa-miR-4721	MIMAT0019835	microRNA	34503528	2021	A direct negative feedback loop of miR-4721 or FOXA1 or Nanog promotes nasopharyngeal cell stem cell enrichment and metastasis	nasopharyngeal carcinoma (NPC)	Further, the sphere formation ability was enhanced in overexpressing miR-4721 HONE1 and SUNE1 cells. We found that miR-4721, FOXA1 and Nanog control their expressions through a negative feedback loop and then activate the downstream regulator of stem cell signaling to promote the enrichment and metastasis of NPC stem cells.	Upregulation	HONE1, SUNE1	Human	500
hsa-miR-451b	MIMAT0019840	microRNA	33725258	2021	The Effect of hsa-miR-451b Knockdown on Biological Functions of Gastric Cancer Stem-Like Cells	gastric cancer (GC)	Upregulation of the KLF4 and SOX2 and downregulation of the CD44, OCT3 or 4, and NANOG decreased Self-renewal ability of gastric cancer stem cells under hsa-miR-451b inhibition. Even, under hsa-miR-451b inhibition, downregulation of Akt, PI3K, Bcl-2 and PCNA as well as upregulation of Bax and CASP3 revealed a movement towards apoptosis in MKN-45 stem-like cells.	Upregulation	MKN-45	Human	494
hsa-miR-5188	MIMAT0021119	microRNA	31604679	2020	Timeless-Stimulated miR-5188-FOXO1 or beta-Catenin-c-Jun Feedback Loop Promotes Stemness via Ubiquitination of beta-Catenin in Breast Cancer	breast cancer (BRCA)	MiR-5188 was upregulated in breast cancer and was positively correlated with poor patient prognosis. miR-5188 exerted an oncogenic effect by inducing breast cancer stemness, proliferation, metastasis, and chemoresistance in vitro and in vivo.	Upregulation	MCF-7, MDA-MB-468	Human	524
hsa-miR-5188	MIMAT0021119	microRNA	31695788	2019	HBX-induced miR-5188 impairs FOXO1 to stimulate beta-catenin nuclear translocation and promotes tumor stemness in hepatocellular carcinoma	hepatocellular carcinoma (HCC)	MiR-5188 was shown to be upregulated and confer poor prognosis. MiR-5188 directly targets FOXO1, which interacts with beta-catenin in the cytoplasm to reduce the nuclear translocation of beta-catenin and promotes the activation of Wnt signaling and downstream tumor stemness, EMT, and c-Jun.	Upregulation	Hep3B, Huh7	Human	525
hsa-miR-660-3p	MIMAT0022711	microRNA	35045883	2022	circFARP1 enables cancer-associated fibroblasts to promote gemcitabine resistance in pancreatic cancer via the LIF or STAT3 axis	pancreatic ductal adenocarcinoma (PDAC)	We found that incubation with conditioned media from miR-660-3p-silenced CAFs enhanced the proliferation, colony formation, sphere formation, and apoptosis resistance of Panc-1 and MiaPaCa-2 cells under GEM treatment. Consistently, upregulating miR-660-3p partially weakened the promoting effects of circFA1P1-overexpressing CAFs on proliferation, sphere formation, and apoptosis resistance under GEM treatment conditions.	Downregulation	Panc-1, MiaPaCa-2	Human	546
hsa-miR-216a-3p	MIMAT0022844	microRNA	34852712	2021	Circular RNA circFLNA inhibits the development of bladder carcinoma through microRNA miR-216a-3p or BTG2 axis	bladder cancer (BLCA)	Downregulated circFLNA and BTG2 expression and upregulated miR-216a-3p were found in both BCa tissues and cell lines. The results showed that miR-216a-3p reversed the inhibitory effect of circFLNA on sphere-forming efficiency, and number and diameter of spherical pellets, and reversed circFLNA-caused inhibition of stem cell markers, CD44, OCT4, and SOX2.	Upregulation	5638	Human	384
hsa-miR-216a-3p	MIMAT0022844	microRNA	30970511	2019	Limonin attenuates the stemness of breast cancer cells via suppressing MIR216A methylation	breast cancer (BRCA)	Limonin decreased MIR216A methylation level and thus increased miR-216a-3p expression. Additionally, miR-216a-3p overexpression significantly decreased the capacity of spheroid formation, characterized as the decrease of spheroid size and number, and suppressed ALDH1 activity. MiR-216a-3p could directly bind to WNT3A and thus inactivated Wnt or beta-catenin pathway.	Downregulation	MCF-7, MDA-MB-231, MCF-10A	Human	385
hsa-miR-216a-3p	MIMAT0022844	microRNA	30876979	2019	BRD4 promotes the stemness of gastric cancer cells via attenuating miR-216a-3p-mediated inhibition of Wnt or beta-catenin signaling	gastric cancer (GC)	We defined a BRD4 or miR-216a-3p or Wnt or beta-catenin pathway in regulating the stemness of gastric cancer cells.	Downregulation	BGC-823, MGC-803	Human	386
hsa-miR-6778-5p	MIMAT0027456	microRNA	32142918	2020	Drosha-independent miR-6778-5p strengthens gastric cancer stem cell stemness via regulation of cytosolic one-carbon folate metabolism	gastric cancer (GC)	MiR-6778-5p or SHMT1 signalling axis is critical to maintain stemness in Drosha downregulated gastric tumours, and interference in miR-6778-5p or SHMT1 signalling may enhance their sensitivity to 5-FU chemotherapy drugs.	Upregulation	MGC-803, BGC-823, NUGC-3	Human	551
hsa-miR-6795-5p	MIMAT0027490	microRNA	33847733	2021	Novel role of LINC01013 or miR-6795-5p or FMNL3 axis in the regulation of hepatocellular carcinoma stem cell features	hepatocellular carcinoma (HCC)	HCC tissues showed increased LINC01013 and FMNL3 expression, while it showed a decreased miR-6795-5p expression as compared to the relative controls.Silencing LINC01013, FMNL3, or overexpression of miR-6795-5p could suppress spheroid and colony formation, proliferation, as well as expression of stemness markers in HepG2 and SNU-182 cells.	Downregulation	HepG2, SNU-182	Human	552
hsa-miR-7156-3p	MIMAT0028223	microRNA	33162825	2020	A novel miR-7156-3p-HOXD13 axis modulates glioma progression by regulating tumor cell stemness	glioma	The expression of miR-7156-3p is significantly decreased in glioma tissues compared to the normal brain.Inhibition of miR-7156-3p effectively stimulates glioma cell stemness, invasion, and growth.MiR-7156-3p regulates glioma cell stemness, invasion, and growth by mediating HOXD13.	Downregulation	U373, SW1783	Human	558
ASAP1-IT1		lncRNA	28895409	2017	Long noncoding RNA ASAP1-IT1 promotes cancer stemness and predicts a poor prognosis in patients with bladder cancer	bladder cancer (BLCA)	To further characterize the role of ASAP1-IT1 in UBC cells, we knocked down ASAP1-IT1 by 2 different siRNAs in T24 cells. In these two groups, we found that depletion of ASAP1-IT1 significantly reduced the sphere number by sphere formation assay. The sizes of spheres in two ASAP1-IT1 knockdown groups were also smaller than those in control group . As ALDHhigh or CD44+ cancer cell subpopulations were generally considered as CSC population in multiple cancers, we examined the CSCs population changes in UBC cells by flow cytometry, when ASAP1-IT1 was knocked down. Compared with control group, ASAP1-IT1 depletion significantly and remarkably reduced the ALDHhigh population, from 11.4 percentage to 5.1 percentage and 5.4 percentage. The CD44+ subpopulation was also reduced from 21.7percentage to 1.93percentage and 1.96percentage. The expression levels of ALDH1A1 and CD44, two CSC markers for UBC, were both decreased at mRNA and protein levels in ASAP1-IT1 knockdown group. Taken together, the results above showed that ASAP1-IT1 is required for UBC cell stemness.	Upregulation	J82	Human	7
ATB		lncRNA	32256798	2020	lncRNA-ATB promotes stemness maintenance in colorectal cancer by regulating transcriptional activity of the beta-catenin pathway	colorectal carcinoma (CRC)	Furthermore, results of the sphere formation assay indicated that ATB knockdown significantly impaired sphere formation in HCT116 and HT29 cells. Collectively, the above results demonstrated the positive role of ATB in CRC stemness maintenance.	Upregulation	HCT116, HT29	Human	10
CASC21		lncRNA	34375566	2021	LncRNA CASC21 induces HGH1 to mediate colorectal cancer cell proliferation, migration, EMT and stemness	colorectal carcinoma (CRC)	Moreover, we explored the influence of CASC21 on cell stemness. Experimental result revealed that the sphere formation efficiency of CRC cells was evidently reduced in response to CASC21 knockdown, indicating that CASC21 knockdown repressed the stemness of CRC cells.	Upregulation	SW620, RKO	Human	18
circ_001680		circRNA	32005118	2020	Hsa_circ_001680 affects the proliferation and migration of CRC and mediates its chemoresistance by regulating BMI1 through miR-340	colorectal carcinoma (CRC)	Circ_001680 was more highly expressed in of CRC tissue than in matched adjacent normal tissues from the same patients. The results of the sphere formation assay demonstrated that the circ_001680-overexpressing cells could form more viable spheres, whereas the number of spheres was significantly reduced through the upregulation of miR-340 in circ_001680-overexpressing cells.	Upregulation	SW480, HCT116	Human	32
circ_002178		circRNA	32951449	2020	Hsa_circ_002178 Promotes the Growth and Migration of Breast Cancer Cells and Maintains Cancer Stem-like Cell Properties Through Regulating miR-1258 or KDM7A Axis	breast cancer (BRCA)	The expression levels of circ_002178 in cancer tissues or BrCa cells were significantly upregulated. Overexpression of circ_002178 contributed to the formation of microspheres, the elevated protein levels of stemness marker, growth, invasion, and migration of BrCa cells.	Upregulation	SUM159PT, MDA-MB-231	Human	33
circ_DCAF6		circRNA	32668286	2020	Circ_DCAF6 potentiates cell stemness and growth in breast cancer through GLI1-Hedgehog pathway	breast cancer (BRCA)	qRT-PCR clarified the high level of circ_DCAF6 in BC cells. BC cells presented suppressed proliferation and stemness in the absence of circ_DCAF6. The stemness of T47D and MDA-MB-231 cells were suppressed in the absence of circ_DCAF6, characterized with decreased sphere numbers.	Upregulation	MDA-MB-231, T47D	Human	38
circ_POLA2		circRNA	32511866	2020	CircRNA circ_POLA2 promotes lung cancer cell stemness via regulating the miR-326 or GNB1 axis	lung cancer (LC)	Circ_POLA2 was highly expressed in lung cancer tissues and predicted a poor prognosis in lung cancer patients. Knockdown of circ_POLA2 inhibited the stemness of lung cancer cells, which is evident by the decreased sphere-formation ability, ALDH1 activity, and stemness marker expression. Circ_POLA2 promotes lung cancer cell stemness and progression via regulating the miR-326 or GNB1 axis.	Upregulation	A549, H1650	Human	39
circAGFG1		circRNA	32681092	2020	CircAGFG1 drives metastasis and stemness in colorectal cancer by modulating YY1 or CTNNB1	colorectal carcinoma (CRC)	CircAGFG1 was upregulated in CRC cell lines. CircAGFG1 silencing significantly suppressed cell proliferation, migration, invasion, and stemness, while promoted cell apoptosis in CRC. In addition, sphere formation efficiency was decreased after circAGFG1 knockdown. CD133 (a typical marker for stemness) positive cell proportion also declined after circAGFG1 silencing. CircAGFG1 modulated YY1 or CTNNB1 axis to drive metastasis and stemness in CRC by sponging miR-4262 and miR-185-5p.	Upregulation	SW480, HCT116	Human	40
circCD151		circRNA	34368867	2021	circCD151 promotes GLI2 expression by regulating miR-30d-5p and enhancing proliferation, invasion and stemness of lung cancer	lung cancer (LC)	The relative expression level of circCD151 in lung cancer tissues was significantly higher compared with that in adjacent tissues. In A549 and NCI-H292 cells, silencing circCD151 decreased cell activity and clonal formation ability and invasion ability was also significantly decreased. CircCD151 could promote the malignant proliferation of lung adenocarcinoma by targeting miR-30d-5p and upregulating GLI2 expression.	Upregulation	A549, NCI-H292	Human	41
circCD226		circRNA	35946568	2022	Identification of exosomal circRNA CD226 as a potent driver of nonsmall cell lung cancer through miR-1224-3p or high mobility group AT-hook 2 axis	non-small cell lung cancer (NSCLC)	The abundance of circCD226 was elevated in serum exosomes, tissues and cells of NSCLC. Loss of circCD226 impeded cell proliferation, migration, invasion and stemness in vitro, as well as tumor growth in vivo. Furthermore, deficiency of circCD226 diminished formed sphere sizes and inhibited OCT4 and Nanog expression levels in A549 and H1299 cells, indicating that knocking down circCD226 weakens NSCLC cell stemness.	Upregulation	A549, H1299	Human	42
circEPHB4		circRNA	33085838	2021	CircRNA EPHB4 modulates stem properties and proliferation of gliomas via sponging miR-637 and up-regulating SOX10	glioma	CircEPHB4 (hsa_circ_0081519) and SOX10 were up-regulated and microRNA (miR)-637 was down-regulated in glioma tissues and cell lines. The neurosphere assay showed that down-regulating circEPHB4 level significantly reduced the number of neurospheres, whereas up-regulating its level markedly promoted neurosphere formation. CircEPHB4 up-regulated SOX10 and Nestin by directly sponging miR-637, thereby stimulating stemness, proliferation and glycolysis of glioma cells.	Upregulation	SHG-44, LN229	Human	43
circFARP1		circRNA	35045883	2022	circFARP1 enables cancer-associated fibroblasts to promote gemcitabine resistance in pancreatic cancer via the LIF or STAT3 axis	pancreatic ductal adenocarcinoma (PDAC)	Silencing or overexpressing circFARP1 in CAFs altered the ability of CAFs to induce tumor cell stemness and GEM resistance via leukemia inhibitory factor (LIF). CircFARP1 upregulated LIF expression by sponging miR-660-3p. Decreasing circFARP1 levels and neutralizing LIF significantly suppressed PDAC growth and GEM resistance in patient-derived xenograft models. The circFARP1 or CAV1 or miR-660-3p or LIF axis is critical for CAF-induced GEM resistance in PDAC.	Upregulation	Panc-1, MiaPaCa-2	Human	44
circFAT1		circRNA	34314629	2022	Overexpression of circRNA circFAT1 in Endometrial Cancer Cells Increases Their Stemness by Upregulating miR-21 Through Methylation	endometrial cancer (EC)	Cell stemness assay was performed to investigate the role of circFAT1 and miR-21 in regulating the stemness of both RL95-2 and HEC-1-A cells. The percentage of CD133+ cells represents cell stemness. The results showed that overexpression of circFAT1 and miR-21 increased cell stemness, and inhibitor of miR-21 decreased cell stemness.Moreover, inhibitor of miR-21 reduced the effects of overexpression of circFAT1 on cell stemness.	Upregulation	RL95-2, HEC-1-A	Human	45
circFLNA		circRNA	34852712	2021	Circular RNA circFLNA inhibits the development of bladder carcinoma through microRNA miR-216a-3p or BTG2 axis	bladder cancer (BLCA)	Downregulated circFLNA and BTG2 expression and upregulated miR-216a-3p were found in both BCa tissues and cell lines. Specifically, overexpression of circFLNA could significantly reduce the sphere-forming efficiency, and the number and diameter of spherical pellets in BCa cells. Further, according to Western blot results, in BCa cells, overexpression of circFLNA led to a significant decrease in the expression of stem cell markers, CD44, OCT4, and SOX2.	Downregulation	5637	Human	46
circ-HSP90A		circRNA	35750765	2023	Circ-HSP90A expedites cell growth, stemness, and immune evasion in non-small cell lung cancer by regulating STAT3 signaling and PD-1 or PD-L1 checkpoint	non-small cell lung cancer (NSCLC)	Circ-HSP90A was up-regulated in NSCLC cells. Sphere formation assays depicted that circ-HSP90A defciency reduced the sphere formation efciency. Circ-HSP90A promoted cell growth, stemness, and immune evasion in NSCLC through regulating STAT3 signaling and programmed cell death 1 (PD-1) or PD-L1 checkpoint.	Upregulation	H1299, A549	Human	48
circLPAR3		circRNA	34528144	2022	Cell Carcinoma Through Regulating the miR-643 or HMGB2 Network	oral squamous cell carcinoma (OSCC)	CircLPAR3 was highly expressed in OSCC tissues and cells. CircLPAR3 silencing suppressed OSCC cell proliferation, metastasis and stemness, while promoted apoptosis. In addition, downregulated circLPAR3 markedly repressed the migrated and invaded cell numbers, as well as reduced the sphere percentage rate of Cal-27 and SCC9 cells. CircLPAR3 contributed to OSCC malignant progression through regulating the miR-643 or HMGB2 axis.	Upregulation	Cal-27, SCC9	Human	50
circNCAPG		circRNA	36635261	2023	The U2AF65 or circNCAPG or RREB1 feedback loop promotes malignant phenotypes of glioma stem cells through activating the TGF-beta pathway	glioma	CircNCAPG can promote the malignant phenotype of GSCs in vitro. CircNCAPG was overexpressed and indicated the poor prognosis in glioma patients. Further neurosphere formation assay and limiting dilution neurosphere formation assay showed that the sphere formation capacity in circNCAPG knockdown GSCs was obviously diminished, whereas it increased dramatically in circNCAPG-overexpressed GSCs. CircNCAPG interacted with and stabilized RREB1, as well as stimulated RREB1 nuclear translocation to activate TGF-beta1 signaling pathway.	Upregulation	U87, U251	Human	51
circNDC80		circRNA	36635757	2023	CircNDC80 promotes glioblastoma multiforme tumorigenesis via the miR-139-5p or ECE1 pathway	glioblastoma (GBM)	When compared to NBT, glioblastoma tissue had a higher level of circNDC80 expression. In functional assays, circNDC80 promoted glioblastoma cell proliferation, migration, and invasion, while sustaining the stemness and fostering the self-renewal of glioma stem cells. CircNDC80 is an oncogenic factor that promotes glioblastoma through the miR-139-5p or ECE1 pathway.	Upregulation	U251, LN229, U118, U87, T98G	Human	52
circ-NOTCH1		circRNA	31943342	2020	miR-449c-5p availability is antagonized by circ-NOTCH1 for MYC-induced NOTCH1 upregulation as well as tumor metastasis and stemness in gastric cancer	gastric cancer (GC)	Circ-NOTCH1 exhibited increased expression in GC tissues and cells. Suppression of circ-NOTCH1 inhibited cell migration, invasion, tumor spheroids number, and side population ratio. Circ-NOTCH1 promoted metastasis and stemness in GC by targeting miR-449c-5p or MYC or NOTCH1 axis.	Upregulation	AGS, BGC-823	Human	53
circPCBP2		circRNA	35579082	2022	CircPCBP2 promotes the stemness and chemoresistance of DLBCL via targeting miR-33a or b to disinhibit PD-L1	diffuse large B-cell lymphoma (DLBCL)	CircPCBP2 was upregulated in human DLBCL specimens and cultured DLBCL cells while miR-33a or b was reduced. Knockdown of circPCBP2 or miR-33a or b overexpression inhibited the stemness of DLBCL cells and promoted cancer cell apoptosis upon CHOP treatment. CircPCBP2 enhances DLBCL cell stemness but suppresses its sensitivity to CHOP via sponging miR-33a or b to disinhibit PD-L1 expression.	Upregulation	U2932, OCI-LY3, SU-DHL-3, NU-DUL-1	Human	54
circPIP5K1A		circRNA	34774083	2021	Circular RNA circPIP5K1A contributes to cancer stemness of osteosarcoma by miR-515-5p or YAP axis	osteosarcoma (OS)	CircPIP5K1A expression was significantly enhanced in clinical osteosarcoma tissues compared with the adjacent normal tissues. The sphere formation abilities of MG63 and 143B cells were repressed by the depletion of circPIP5K1A. Besides, the CD133+CD44+ cell population of MG63 and 143B cells was reduced by circPIP5K1A knockdown. We found that the depletion of circPIP5K1A or miR-515-5p mimic could attenuate the sphere formation abilities of MG63 and 143B cells, and the inhibition of miR-515-5p or YAP overexpression could rescue the attenuation effect of circPIP5K1A MG63 and 143B cells.	Upregulation	MG63, 143B	Human	55
circPTN		circRNA	31511040	2019	circPTN sponges miR-145-5p or miR-330-5p to promote proliferation and stemness in glioma	glioma	CircPTN was significantly higher expression in glioma tissues and glioma cell lines, compared with NBT and HEB (human astrocyte). The results showed that the sphere percentage was significantly increased in the circPTN group compared with the EV group. In contrast, after interfering with circPTN expression, the sphere percentage was significantly decreased.	Upregulation	G15, U87-GSC, U251-GSC	Human	56
circRPPH1		circRNA	36190453	2023	CircRPPH1 promotes the stemness of gastric cancer cells by targeting miR-375 or SLC7A11 axis	gastric cancer (GC)	In addition, the sphere-formation ability was significantly attenuated by circRPPH1 knockdown, as evident by the reduction of sphere size and number. CircRPPH1 acted as an miR-375 sponge to positively regulate SLC7A11 expression, which has been confirmed to be the direct target of miR-375 in gastric cancer, and thus regulated ferroptosis. Moreover, circRPPH1 promoted the stemness of gastric cancer cells dependent on the miR-375 or SLC7A11.	Upregulation	MKN-45, AGS	Human	57
circSETD3		circRNA	34288821	2021	Circular RNA circSETD3 hampers cell growth, migration, and stem cell properties in bladder cancer through sponging miR-641 to upregulate PTEN	bladder cancer (BLCA)	CircSETD3 was remarkably downregulated in the cancerous clinical tissues and cell lines in BLCA patients with larger tumor size, advanced clinical stages, positive lymph metastasis and worse prognosis. Furthermore, microsphere assay showed that the number of sphere formation was reduced by overexpression of circSETD3. CircSETD3 acted as a tumor suppressor to suppress BLCA cell proliferation, migration, EMT and stemness, and the underlying mechanisms,circSETD3 sponged miR-641 to upregulate PTEN, resulting in the blockage of BLCA progression.	Downregulation	T24, UMUC3	Human	58
circVAPA		circRNA	33619796	2021	CircVAPA exerts oncogenic property in non-small cell lung cancer by the miR-876-5p or WNT5A axis	non-small cell lung cancer (NSCLC)	Our findings demonstrated high expression of circVAPA in tissues and cell lines of NSCLC. Sphere formation assay showed that inhibition of circVAPA decreased the number of spheres in H1299 and H1975 cells. Moreover, the levels of stemness markers (SOX2 and OCT4 and Nanog) were inhibited by downregulation of circVAPA, demonstrating that circVAPA knockdown suppressed cell stemness maintenance in NSCLC. CircVAPA promotes aggressive phenotypes of NSCLC cells by the miR-876-5p or WNT5A axis activating Wnt or beta-catenin signaling.	Upregulation	H1299, H1975	Human	59
circZNF609		circRNA	32398664	2020	CircZNF609 enhances hepatocellular carcinoma cell proliferation, metastasis, and stemness by activating the Hedgehog pathway through the regulation of miR-15a-5p or 15b-5p and GLI2 expressions	hepatocellular carcinoma (HCC)	CircZNF609 was conspicuously overexpressed and featured with loop structure in HCC. Additionally, the sphere formation ability of HCCLM3 and MHCC-97H cells was restrained by circZNF609 deficiency. Decreased expression of circZNF609 suppressed cell proliferation, metastasis and stemness, whereas induced cell apoptosis in HCC. CircZNF609 enhances HCC cell proliferation, metastasis, and stemness by activating the Hedgehog pathway through the regulation of miR-15a-5p or 15b-5p and GLI2 expressions.	Upregulation	HCCLM3, MHCC-97H	Human	60
cricN4BP2L2		circRNA	35752345	2022	CAFs-secreted exosomal cricN4BP2L2 promoted colorectal cancer stemness and chemoresistance by interacting with EIF4A3	colorectal carcinoma (CRC)	LoVo or OXA cells incubated with CAFs-exo or sh-cricN4BP2L2 had decreased cell proliferation and sphere formation, and increased apoptosis when compared with CAFsexo or sh-NC group. CAFs-exo cricN4BP2L2 promoted the CRC cells stemness and oxaliplatin resistance through EIF4A3 or PI3K or AKT or mTOR pathway.	Upregulation	LoVo	Human	61
DDIT4-AS1		lncRNA	36056355	2022	cancer stemness and suppresses chemosensitivity by activating the mTOR pathway	pancreatic cancer (PaCa)	DDIT4-AS1 was upregulated in PDAC and positively correlated with a poor prognosis. DDIT4-AS1 knockdown reduced the ability of PDAC cells to form primary and secondary spheroids. However, forced expression of DDIT4-AS1 increased primary and secondary spheroid formation. The ALKBH5-mediated m6A modification led to DDIT4-AS1 overexpression in PDAC, and DDIT-AS1 increased cancer stemness and suppressed chemosensitivity to GEM by destabilizing DDIT4 and activating the mTOR pathway.	Upregulation	BxPC-3, SW1990	Human	67
HOXATs		lncRNA	34805277	2021	A Pan-Cancer Landscape of HOX-Related lncRNAs and Their Association With Prognosis and Tumor Microenvironment	Pan-Cancer	HOXB-AS1 expression was significantly higher in GBM than in lower grade glioma tissues. Sphere formation assay revealed that HOXB-AS1 knockdown inhibited spheroid formation in GSCs, indicating that HOXB-AS1 supports cancer stem cell growth.	Upregulation	U251, HS683	Human	123
IPW		lncRNA	35078502	2022	LncRNA IPW inhibits growth of ductal carcinoma in situ by downregulating ID2 through miR-29c	ductal carcinoma in situ (DCIS)	We found that IPW expression significantly decreased sphere formation ability in DCIS.com, SUM225 and S2 cells. Ectopic expression of IPW in DCIS cells strongly inhibited cell proliferation, colony formation and cell cycle progression while silencing IPW in primary breast cells promoted their growth. MiR-29c negatively regulated a stemness promoting gene, ID2, and diminished self-renewal ability of DCIS cells.	Downregulation	DCIS.com, SUM225	Human	127
IPW		lncRNA	35078502	2022	LncRNA IPW inhibits growth of ductal carcinoma in situ by downregulating ID2 through miR-29c	ductal carcinoma in situ (DCIS)	We found that IPW expression significantly decreased sphere formation ability in DCIS.com, SUM225 and S2 cells. Ectopic expression of IPW in DCIS cells strongly inhibited cell proliferation, colony formation and cell cycle progression while silencing IPW in primary breast cells promoted their growth. MiR-29c negatively regulated a stemness promoting gene, ID2, and diminished self-renewal ability of DCIS cells.	Downregulation	S2	Mouse	128
KB-1980E6.3		lncRNA	33469161	2021	A novel hypoxic long noncoding RNA KB-1980E6.3 maintains breast cancer stem cell stemness via interacting with IGF2BP1 to facilitate c-Myc mRNA stability	breast cancer (BRCA)	LncRNA KB-1980E6_3 knockdown attenuated tumor growth and tumor weight of xenograft mice. LncRNA KB-1980E6_3 maintains the stemness of BCSCs through lncRNA KB-1980E6.3 or IGF2BP1 or c-Myc axis.	Upregulation	BT549, Hs578T	Human	129
LINC-DYNC2H1-4		lncRNA	28703793	2017	LINC-DYNC2H1-4 promotes EMT and CSC phenotypes by acting as a sponge of miR-145 in pancreatic cancer cells	pancreatic ductal adenocarcinoma (PDAC)	LINC-DYNC2H1-4 was upregulated in pancreatic cancer cell line BxPC-3-Gem with acquired gemcitabine resistance. Knockdown of LINC-DYNC2H1-4 decreased the invasive behavior of BxPC-3-Gem cells while ectopic expression of LINC-DYNC2H1-4 promoted the acquisition of EMT and stemness of the parental sensitive cells.	Upregulation	BxPC-3, AsPC-1, PANC-1	Human	170
LINC-ZNF469-3		lncRNA	29755127	2018	A novel long non-coding RNA LINC-ZNF469-3 promotes lung metastasis through miR-574-5p-ZEB1 axis in triple negative breast cancer	breast cancer (BRCA)	LINC-ZNF469-3 was highly expressed in lung-metastatic LM2-4175 TNBC cells and overexpression of LINC-ZNF469-3 enhanced invasion ability and stemness properties in vitro and lung metastasis in vivo. LINC-ZNF469-3 promotes lung metastasis of TNBC through miR-574-5p-ZEB1 signaling axis.	Upregulation	MDA-MB-231, LM2-4175	Human	174
lnc030		lncRNA	33511005	2020	A Novel Long Non-Coding RNA lnc030 Maintains Breast Cancer Stem Cell Stemness by Stabilizing SQLE mRNA and Increasing Cholesterol Synthesis	breast cancer (BRCA)	Lnc030 is highly expressed in BCSCs in vitro and in vivo, and maintain BCSC stemness via the lnc030-SQLE-cholesterol synthesis pathway. Indeed, increased ALDH activity was detected in lnc030-high breast cancer tissues compared with that in lnc030-low tumor tissues, and the breast cancer cells isolated from breast tumor with high lnc030 expression showed higher mammosphere-formation abilities in comparison to those with low lnc030 expression.	Upregulation	Hs578T, BT549	Human	177
lnc273-31		lncRNA	31455383	2019	P53-R273H mutation enhances colorectal cancer stemness through regulating specific lncRNAs	colorectal carcinoma (CRC)	Lnc273-31 and lnc273-34 were significantly highly expressed in CRC tissues with p53-R273H mutation compared to those with wildtype p53. Furthermore, knocking down of lnc273-31 or lnc273-34 significantly impaired the spheroid formation abilities, including spheroid size and spheroid number, indicating the attenuated generation of colorectal CSCs and self-renewal capabilities. Lnc273-31 or lnc273-34 depletion dramatically diminished colorectal cancer migration, invasion, cancer stem cell self-renewal and chemoresistance in vitro.	Upregulation	HCT116	Human	178
lnc273-34		lncRNA	31455383	2019	P53-R273H mutation enhances colorectal cancer stemness through regulating specific lncRNAs	colorectal carcinoma (CRC)	Lnc273-31 and lnc273-34 were significantly highly expressed in CRC tissues with p53-R273H mutation compared to those with wildtype p53. Furthermore, knocking down of lnc273-31 or lnc273-34 significantly impaired the spheroid formation abilities, including spheroid size and spheroid number, indicating the attenuated generation of colorectal CSCs and self-renewal capabilities. Lnc273-31 or lnc273-34 depletion dramatically diminished colorectal cancer migration, invasion, cancer stem cell self-renewal and chemoresistance in vitro.	Upregulation	HCT116	Human	179
lncCCAT1		lncRNA	31695775	2019	LncCCAT1 Promotes Breast Cancer Stem Cell Function through Activating WNT or beta-catenin Signaling	breast cancer (BRCA)	LncCCAT1 is markedly upregulated in breast cancer tissues BCSCs and is correlated with poor outcomes in breast cancer patients. Overexpression of LncCCAT1 contributes to the proliferation, stemness, migration and invasion capacities of BCSCs. Importantly, LncCCAT1 overexpression dramatically increased the sphere-formation efficiency of breast cancer cells, while LncCCAT1-KO impaired self-renewal capacity on serial passaging.	Upregulation	MCF-7, MDA-MB-231	Human	180
lnc-cCSC1		lncRNA	31680315	2020	LncRNA-cCSC1 modulates cancer stem cell properties in colorectal cancer via activation of the Hedgehog signaling pathway	colorectal carcinoma (CRC)	The depletion of lncRNA-cCSC1 markedly inhibited the self-renewal capacity of the CRCSCs and reduced their drug resistance to 5-fluorouracil. Interestingly, knockdown of lncRNA-cCSC1 significantly inhibited tumor spheres number and volume. LncRNA-cCSC1 may regulate CSC-like properties via the Hh signaling pathway.	Upregulation	HT29, HCT116	Human	181
lncGata6		lncRNA	30224759	2018	LncGata6 maintains stemness of intestinal stem cells and promotes intestinal tumorigenesis	colorectal carcinoma (CRC)	LncGata6 is highly expressed in ISCs. LncGata6 knockout or conditional knockout in ISCs impairs the stemness of ISCs and epithelial regeneration.	Upregulation	LGR5	Human	182
lnc-LET		lncRNA	28839463	2017	TGFbeta1 Promotes Gemcitabine Resistance through Regulating the LncRNA-LET or NF90 or miR-145 Signaling Axis in Bladder Cancer	urinary bladder cancers (UBCs)	Depletion of lncRNA-LET significantly increased both cancer incidence and tumor volumes. Overexpression of lncRNA-LET reversed TGFbeta1-induced cancer stemness, with increase of sphere number and the expression levels of CSC markers. Overexpressed lncRNA-LET in T24 cells, and as expected that overexpression of lncRNA-LET reduced the levels of the stemness markers. LncRNA-LET is essential and sufficient for maintenance of UBC stemness, whereas forced overexpression of lncRNA-LET could partially reverse chemoresistance in UBC.	Downregulation	T24, 5637	Human	183
lnc-PDZD7		lncRNA	30786928	2019	Lnc-PDZD7 contributes to stemness properties and chemosensitivity in hepatocellular carcinoma through EZH2-mediated ATOH8 transcriptional repression	hepatocellular carcinoma (HCC)	Lnc-PDZD7 is frequently upregulated in HCC tissues.Lnc-PDZD7 promotes stemness properties and suppresses chemosensitivity though the miR-101 or EZH2 or ATOH8 pathway.	Downregulation	Bel-7402, HepG2	Human	184
lnc-PKD2-2-3		lncRNA	31059014	2019	lnc-PKD2-2-3, identified by long non-coding RNA expression profiling, is associated with pejorative tumor features and poor prognosis, enhances cancer stemness and may serve as cancer stem-cell marker in cholangiocarcinoma (CCA)	cholangiocarcinoma (CCA)	Lnc-PKD2-2-3 was upregulated in CCA. In vitro, and increased CD44, CD133 and OCT4 expression as well as the CD44+CD133+ cell proportion, raised the sphere formation efficiency and enhanced drug resistance to 5-FU in TFK-1 and Huh-28 cells.Lnc-PKD2-2-3 was positively correlated with CSC markers in CCA tumor tissues.	Upregulation	R-TFK-1, R-Huh-28	Human	185
lncROPM		lncRNA	34715882	2021	A novel lncRNA ROPM-mediated lipid metabolism governs breast cancer stem cell properties	breast cancer (BRCA)	LncROPM is highly expressed in BCSCs. LncROPM was positively correlated with Sox2, Oct4, and ALDH1A1 expression in breast tumor tissues.	Upregulation	BT-549, MCF-7	Human	186
lnc-ZNF281		lncRNA	30509101	2019	Novel lncRNA-ZNF281 regulates cell growth, stemness and invasion of glioma stem-like U251s cells	glioma	The expression of lncRNA-ZNF281 was lower in glioma stem-like cells (U251s), lncRNA-ZNF281 inhibits the self-renewing ability and invasion of GSCs in vitro and in vivo and can reduce tumorigenicity in the glioma stem-like cell (U251s).	Downregulation	U251	Human	188
LOC100507144		lncRNA	34882869	2022	LncRNA LOC100507144 acts as a novel regulator of CD44 or Nanog or Sox2 or miR-302 or miR-21 axis in colorectal cancer	colorectal carcinoma (CRC)	The expression of LOC100507144 transcript was substantially higher in tumors with advanced stages, lymph node metastasis, and vascular invasion. LOC100507144 promotes stemness features of colorectal cancer stem cells. LOC100507144 could enhance CRC progression and metastasis through regulation of the CD44 or Nanog or Sox2 or miR-302 or miR-21 axis.	Upregulation	SW480, HT29	Human	189
hsa-miR-129-2-5p		microRNA	36077697	2022	DNMT3A or miR-129-2-5p or Rac1 Is an Effector Pathway for SNHG1 to Drive Stem-Cell-like and Invasive Behaviors of Advanced Bladder Cancer Cells	bladder cancer (BLCA)	The reduced binding of miR-129-2 to the 3'-UTR of Rac1 mRNA leads to the stabilization of Rac1 mRNA and increased levels of Rac1 protein, which then stimulates MIBC cell sphere formation and invasion. SNHG1 or DNMT3A or miR-129-2-5p or Rac1 effector pathway drives stem-cell-like and invasive behaviors in MIBC.	Upregulation	T24T, UMUC3	Human	244
hsa-miR-302-367		microRNA	28358371	2017	Cell-based therapy using miR-302-367 expressing cells represses glioblastoma growth	glioblastoma (GBM)	We engineered primary glioma cells to stably express the miR-302-367. Remarkably, these cells altered, in a paracrine-dependent manner, the expression of stemness markers, the proliferation and the tumorigenicity of neighboring glioblastoma cells.	Downregulation	TG1, TG6, GB1	Human	413
hsa-miR-30-5p		microRNA	30338942	2019	MiR-30-5p suppresses cell chemoresistance and stemness in colorectal cancer through USP22 or Wnt or beta-catenin signaling axis	colorectal carcinoma (CRC)	MiR-30-5p overexpression reduced the number of CD133 + Caco2 cell spheres. Furthermore, miR-30-5p overexpression significantly inhibited HCT15 stem cell proliferation, as determined by MTT assays. MiR-30-5p is normally decreased in CD133 + CRC cells, miR-30-5p overexpression significantly reduces expression of stem cell markers CD133 and Sox2, sphere formation, and cell proliferation. MiR-30-5p attenuates the expression of Wnt or beta-catenin signaling target genes (Axin2 and MYC), Wnt luciferase activity, and beta-catenin protein levels in CRC stem cells.	Downregulation	Caco2, HCT15	Human	418
hsa-miR-365-3p		microRNA	30782177	2019	A novel miR-365-3p or EHF or keratin 16 axis promotes oral squamous cell carcinoma metastasis, cancer stemness and drug resistance via enhancing beta5-integrin or c-met signaling pathway	oral squamous cell carcinoma (OSCC)	MiR-365-3p targets EHF to inhibit OSCC migration, invasion, and metastasis through KRT16. Depletion of KRT16 impaired migration, invasion, metastasis, and cancer stemness of OSCC cells.	Downregulation	OC-3, C9-IV3	Human	462
hsa-miR-965		microRNA	32586376	2020	Shrimp miR-965 induced the human melanoma stem-like cell apoptosis and inhibited their stemness by disrupting the MCL-1-ER stress-XBP1 feedback loop in a cross-species manner	melanoma	shrimp miR-965, could regulate MSLC stemness and survival by targeting MCL-1 and disrupting the balance of MCL-1-ER stress-XBP1 feedback loop. Shrimp miR-965 mediated consecutive tumorsphere formation inhibition.	Downregulation	MDA-MB-435	Human	575
piRNA-823		piRNA	30979371	2019	Myeloid-derived suppressor cells endow stem-like qualities to multiple myeloma cells by inducing piRNA-823 expression and DNMT3B activation	multiple myeloma	Silencing of piRNA-823 in MM cells reduced the stemness of MMSCs maintained by G-MDSCs, resulting in decreased tumor burden and angiogenesis in vivo.	Upregulation	RPMI8226, NCI-H929	Human	592
RUNX1-IT1		lncRNA	32024815	2020	LncRNA RUNX1-IT1 which is downregulated by hypoxia-driven histone deacetylase 3 represses proliferation and cancer stem-like properties in hepatocellular carcinoma cells	hepatocellular carcinoma (HCC)	Overexpression of RUNX1-IT1 impaired the growth, metastasis and stem-like features of HCC cells in vivo. Intriguingly, RUNX1-IT1 overexpression in MHCC-97H cells repressed the invasive capacity and decreased the number and size of tumourspheres in comparison to MHCC-97H vector control cells.	Downregulation	MHCC-97H	Human	602
SLNCR1		lncRNA	31524254	2019	Long non-coding RNA SLNCR1 regulates non-small cell lung cancer migration, invasion and stemness through interactions with secretory phospholipase A2	non-small cell lung cancer (NSCLC)	SLNCR1 expression levels were upregulated in tumor tissues compared with adjacent healthy tissues of patients with NSCLC. LncRNA SLNCR1 siRNA silencing inhibited, whereas sPLA2 overexpression promoted cell migratory and invasive abilities and stemness.	Upregulation	H1581, H1993	Human	604
SNHG		snoRNA	36159816	2022	Identification and validation of SNHG gene signature to predict malignant behaviors and therapeutic responses in glioblastoma	glioblastoma (GBM)	SNHGclusterA was significantly enriched for the MES subtype, whereas SNHGclusterB was enriched for the PN subtype. The SNHG family was negatively correlated with immunity and positively correlated with stemness. We observed that knockdown of SNHG18 in GSCs resulted in a significant inhibition of tumorsphere expansion.	Upregulation	GSC20, GSC267	Human	605
SPRY4-IT1		lncRNA	31736268	2020	LncRNA SPRY4-IT1 regulates breast cancer cell stemness through competitively binding miR-6882-3p with TCF7L2	breast cancer (BRCA)	SPRY4-IT1 was up-regulated in MCF-7 CSCs compared with MCF-7 cells. SPRY4-IT1 promotes proliferation and stemness of breast cancer cells as well as renewal ability and stemness maintenance of BCSCs by increasing the expression of TCF7L2 through targeting miR-6882-3p.	Upregulation	MCF-7, T47D	Human	621