miRNA	gene	miRNA_log2FC	miRNA_pvalue	gene_log2FC	gene_pvalue	interactions	correlation_beta	correlation_pvalue	PMID	evidence	outcome	cancer
hsa-let-7a-5p	EZH2	-1.37014061604018	3.11451492971224e-14	2.63566539246403	3.78349576722754e-27	miRNAWalker2_validate;miRNATAP	-0.623211924106903	4.21735669867407e-24		NA	NA	NA
hsa-let-7b-5p	EZH2	-1.62016148171663	1.56547487335694e-15	2.63566539246403	3.78349576722754e-27	miRNATAP	-0.558499742000965	7.47257521190597e-25	25611389	Significant inverse correlation between EZH2 and hsa-miR-26a-5p R2=0.56 P=0.0001 and hsa-let-7b-5p R2=0.19 P=0.02 expression was observed in the same samples corroborating the belief of EZH2 being a bona fide target for these two miRNAs in CRC		colorectal cancer
hsa-let-7d-5p	EZH2	-0.618145137285851	6.06067642715858e-05	2.63566539246403	3.78349576722754e-27	miRNATAP	-0.215718677151409	0.00552146599617724		NA	NA	NA
hsa-let-7e-5p	EZH2	-0.749418249305995	7.34668338492227e-05	2.63566539246403	3.78349576722754e-27	miRNATAP	-0.351604423510077	1.64632634550653e-08		NA	NA	NA
hsa-let-7f-5p	EZH2	-0.0523311272618407	0.83407808268787	2.63566539246403	3.78349576722754e-27	miRNATAP	-0.225430354087513	2.13184876045812e-06		NA	NA	NA
hsa-let-7g-5p	EZH2	0.0837630831079359	0.583083118232597	2.63566539246403	3.78349576722754e-27	miRNATAP	-0.264934169758142	0.000806163253395814		NA	NA	NA
hsa-miR-101-3p	EZH2	1.38889039459232	1.96522549511542e-09	2.63566539246403	3.78349576722754e-27	miRNAWalker2_validate;miRTarBase;MirTarget;miRNATAP	-0.178706182654249	0.000420674091113109	25428391;22977606;24002871;26718325;26251675;22108826;24490857;23962556;21818714;25260883;24211739;27620004;22450781;25400732;25190211;24807198;21321380;22094936;21270667	The results showed that mir-101 was down-regulated and EZH2 were upregulated; Subsequently the roles of mir-101 and EZH2 in tumor growth and progression in vitro were tested; Overexpression of mir-101 mimics was able to suppress the expression of EZH2 in XWLC-05 cells; Interleukin-1β subsequently induces the downregulation of mir-101 which may result in the upregulated level of EZH2 and occurrence of lung cancer;Therefore we aimed to ascertain whether or not the overexpression of miR-101 inhibits invasion of lung cancer through regulation of EZH2; In this study the expression of miR-101 was down-regulated and the expression of EZH2 was up-regulated in lung cancer; Overexpression of miR-101 induced a marked reduction in EZH2 mRNA levels in several lung cancer cell lines; miR-101 may be a potent tumor suppressor by altering chromatin structure through repression of EZH2 and may be a potential therapeutic tool for patients with lung cancer;miR-101 in turn inhibits the expression of two subunits of PRC2 EZH2 and EED thus creating a double-negative feedback loop that regulates the process of hepatocarcinogenesis; In addition co-overexpression of c-Myc and EZH2 in HCC samples was closely associated with lower expression of miR-101 P < 0.0001 and poorer prognosis of HCC patients P < 0.01;Reporter gene assays revealed that ectopic expression of EZH2 inhibited the transcriptional activities of miR-101-1 promoter; Moreover our results also demonstrated that similar antitumor effects can be achieved either by ectopic miR-101 or EZH2 silencing in HCC cells; These findings show that elevated EZH2 contributes to miR-101 deregulation in HCC and highlight the coordinated role of miR-101 and EZH2 in hepatocarcinogenesis;MiR-101 is a microRNA involved in a negative feedback circuit with EZH2 in different normal and tumor tissues; To that miR-101 can behave as a tumor suppressor in several cancers by repressing EZH2 expression; We therefore evaluated whether miR-101 is de-regulated in eRMS and investigated its interplaying with EZH2 as well as its role in the in vitro tumorigenic potential of these tumor cells; Herein we report that miR-101 is down-regulated in eRMS patients and in tumor cell lines compared to their controls showing an inverse pattern of expression with EZH2; We also show that miR-101 is up-regulated in eRMS cells following both genetic and pharmacological inhibition of EZH2; In turn miR-101 forced expression reduces EZH2 levels as well as restrains the migratory potential of eRMS cells and impairs their clonogenic and anchorage-independent growth capabilities; This phenomenon is associated to reduced H3K27me3 levels at the same regulatory locus indicating that EZH2 directly targets miR-101 for repression in eRMS cells; Altogether our data show that in human eRMS miR-101 is involved in a negative feedback loop with EZH2 whose targeting has been previously shown to halt eRMS tumorigenicity;Mechanistic investigations revealed that reexpression of miR-101 was sufficient to limit the expression of EZH2 and the proinvasive cell surface adhesion molecule EpCAM;Methyl jasmonate sensitizes human bladder cancer cells to gambogic acid induced apoptosis through down regulation of EZH2 expression by miR 101; Furthermore treatment of bladder cancer cells with a combination of GA and MJ induced synergistic inhibition of the enhancer of zeste homologue 2 EZH2 expression whereas miR-101 expression was up-regulated; Conversely knockdown of miR-101 restored this decreased expression of EZH2 and suppressed the inhibitory effect of GA and MJ on the growth of bladder cancer cells; MJ sensitizes bladder cancer cells to GA-induced apoptosis by down-regulating the expression of EZH2 induced by miR-101;MiR 101 inhibits melanoma cell invasion and proliferation by targeting MITF and EZH2; Functional assays showed that miR-101 suppressed invasion and proliferation - an outcome that could be phenocopied by siRNA knockdown of MITF and EZH2;We explore the role of miR-101 and its interaction with EzH2 in epithelial ovarian carcinoma EOC; CHIP assays revealed that re-expression of miR-101 inhibited the interaction of EzH2 with p21waf1/cip1 promoter;miR 101 regulates expression of EZH2 and contributes to progression of and cisplatin resistance in epithelial ovarian cancer; miR-101 overexpression decreased the expression of EZH2 reduced proliferation and migration of ovarian cancer cells and resensitized drug-resistant cancer cells to cisplatin-induced cytotoxicity suggesting the important role miR-101 plays in ovarian cancer that may be associated with its function as a regulator targeting EZH2;The aim of our study was to investigate the functional role of both miR-101 and EZH2 in human hepatocellular carcinoma HCC; MiR-101 and EZH2 expressions were evaluated in tumor tissues of 99 HCC patients and 7 liver cancer cell lines by real-time PCR; Luciferase reporter assay was employed to validate whether EZH2 represents a target gene of miR-101; MiR-101 expression was significantly downregulated in most of HCC tissues and all cell lines whereas EZH2 was significantly overexpressed in most of HCC tissues and all cell lines; There was a negative correlation between expression levels of miR-101 and EZH2; Luciferase assay results confirmed EZH2 as a direct target gene of miR-101 which negatively regulates EZH2 expression in HCC; Tumor suppressor miR-101 represses HCC progression through directly targeting EZH2 oncogene and sensitizes liver cancer cells to chemotherapeutic treatment;Long non coding RNA XIST regulates gastric cancer progression by acting as a molecular sponge of miR 101 to modulate EZH2 expression;Moreover around 40% of cases showing miR-101 down-regulation displayed concomitant EZH2 over-expression at the RNA and protein levels which in turn was associated with loss/aberrant expression of E-cadherin; In conclusion we show that deletions and/or microdeletions at both miR-101 genomic loci cause mature miR-101 down-regulation subsequent EZH2 over-expression and E-cadherin dysfunction specifically in intestinal-type GC;miR 101 suppresses tumor proliferation and migration and induces apoptosis by targeting EZH2 in esophageal cancer cells; The expression level of miR-101 was inversely correlated to EZH2 protein expression in ESCC cell; These findings suggest that decreased expression of miR-101 might promote metastasis of human ESCC by inducing accumulation of EZH2 protein;In the present study we reported that ectopic overexpression of miR-101 downregulated the expression level of EZH2 and significantly inhibited migration and invasion of osteosarcoma cells; In addition knockdown of EZH2 by siRNA showed the same effect of miR-101 on migration and invasion; To conclude these results indicate that miR-101 may act as a tumor suppressor in osteosarcoma as it has a suppressive role in cell migration and invasion by targeting EZH2;MiR 101 downregulated in retinoblastoma functions as a tumor suppressor in human retinoblastoma cells by targeting EZH2; Finally we found that miR-101 directly inhibited EZH2 expression by targeting its 3'-UTR and EZH2 was upregulated and inversely correlated with miR-101 expression in the retinoblastoma tissues; Thus for the first time we provide convincing evidence that downregulation of miR-101 is associated with tumor aggressiveness in retinoblastoma and inhibits cell growth and proliferation of retinoblastoma cells by targeting EZH2;miR 101 is down regulated in glioblastoma resulting in EZH2 induced proliferation migration and angiogenesis; Here we determined that miR-101 is down-regulated in GBM resulting in overexpression of the miR-101 target PcG protein EZH2 a histone methyltransferase affecting gene expression profiles in an epigenetic manner; Our results indicate that EZH2 has a versatile function in GBM progression and that its overexpression is at least partly due to decreased miR-101 expression;Main objective of the present study is to investigate miR-26a and miR-101 levels which both target EZH2 for their association with molecular pathways and with efficacy of tamoxifen as first-line monotherapy for metastatic breast cancer;In this study we investigate whether miRNA miR-101 regulates EZH2 expression in NSCLC; We evaluated the expression of miR-101 and EZH2 in 20 matched NSCLC and adjacent nontumor lung tissues by reverse-transcriptase polymerase chain reaction and immunohistochemistry respectively; Luciferase reporter assay was used to determine whether miR-101 directly targets EZH2; To assess the effect of miR-101 on NSCLC biological behavior cell proliferation invasion and response to chemotherapy were analyzed using NSCLC cells transfected with miR-101 mimics or transfected with specific small interfering RNA to deplete EZH2 small interfering RNA-EZH2; Reduced expression of miR-101 was associated with overexpression of EZH2 in NSCLC tumor tissues; Transfection of miR-101 mimics significantly suppressed the activity of the luciferase reporter containing wild type but not mutant EZH2 3'-UTR and decreased EZH2 expression in NSCLC cell lines; Therapeutic strategies to rescue miR-101 expression or silence EZH2 may be beneficial to patients with NSCLC in the future	progression;;tumorigenesis;worse prognosis;tumorigenesis;;;;;;progression;drug resistance;progression;progression;;metastasis;cell migration;;progression;;drug resistance	lung cancer;lung cancer;liver cancer;liver cancer;sarcoma;pancreatic cancer;bladder cancer;melanoma;ovarian cancer;ovarian cancer;liver cancer;gastric cancer;gastric cancer;esophageal cancer;sarcoma;retinoblastoma;glioblastoma;breast cancer;lung squamous cell cancer
hsa-miR-139-5p	EZH2	-2.26625553116965	7.22375119369519e-16	2.63566539246403	3.78349576722754e-27	miRanda	-0.302451271314397	4.45008618629251e-14		NA	NA	NA
hsa-miR-150-3p	EZH2	-2.17740259423713	1.4154585312719e-10	2.63566539246403	3.78349576722754e-27	MirTarget;miRNATAP	-0.161500564567485	2.84837083335974e-06		NA	NA	NA
hsa-miR-214-3p	EZH2	-1.1136198715556	3.52054933799089e-05	2.63566539246403	3.78349576722754e-27	miRNAWalker2_validate;miRTarBase	-0.178660658935758	4.67619247071368e-05	21828058;22867052;22962603	Decreased microRNA 214 levels in breast cancer cells coincides with increased cell proliferation invasion and accumulation of the Polycomb Ezh2 methyltransferase; We have shown previously that miR-214 regulates Ezh2 in skeletal muscle and embryonic stem cells; MiR-214 expression was inversely correlated with Ezh2 mRNA and protein levels in breast cancer cell lines and at least one copy of the miR-214 alleles was found to be deleted in 24% 6/25 of primary breast tumors; Experimental increase of miR-214 in breast cancer cell lines correlated with reduction of Ezh2 protein levels a known marker of invasion and aggressive breast cancer behavior; Supporting a direct targeting mechanism miR-214 decreased luciferase activity from a construct containing the Ezh2 3' untranslated region; These findings indicate that reduced miR-214 levels may contribute to breast tumorigenesis by allowing abnormally elevated Ezh2 accumulation and subsequent unchecked cell proliferation and invasion;In Eca109 cells overexpression of miR-98 and miR-214 significantly inhibited the migration and invasion of ESCC cells which was reversed by transfection of EZH2; These findings suggest that decreased expression of miR-98 and miR-214 might promote metastasis of human ESCC by inducing accumulation of EZH2 protein;The enhancer of zeste homologue 2 EZH2 and β-catenin CTNNB1 was identified as two potential direct downstream targets of miR-214 through bioinformatics analysis and experimentally validated the miRNA-target interactions with a dual-firefly luciferase reporter assay; Furthermore the silencing of miR-214 or overexpression of EZH2 increased EpCAM+ stem-like cells through the activation of CTNNB1	tumorigenesis;metastasis;	breast cancer;esophageal cancer;liver cancer
hsa-miR-26a-5p	EZH2	-0.126411409001078	0.440028840408711	2.63566539246403	3.78349576722754e-27	miRNAWalker2_validate;miRTarBase;MirTarget;miRNATAP	-0.552405796444427	1.30452959392404e-14	20952513;23750239;25611389;24452597;26733151;21901171;25494962;27517917;22086681;27562865;22930729;22094936	Pathologically decreased miR 26a antagonizes apoptosis and facilitates carcinogenesis by targeting MTDH and EZH2 in breast cancer; Subsequently MTDH and EZH2 are identified as two direct targets of miR-26a and they are significantly upregulated in breast cancer; MCF7 xenografts with exogenous miR-26a show that a decrease in expression of both MTDH and EZH2 is accompanied by an increase in apoptosis; Our findings suggest that miR-26a functionally antagonizes human breast carcinogenesis by targeting MTDH and EZH2;MiR-26a has been reported as a tumor suppressor microRNA in breast cancer which is attributed mainly to targeting of MTDH and EZH2 however the expression profile and therapeutic potential of miR-26a is still unclear;Significant inverse correlation between EZH2 and hsa-miR-26a-5p R2=0.56 P=0.0001 and hsa-let-7b-5p R2=0.19 P=0.02 expression was observed in the same samples corroborating the belief of EZH2 being a bona fide target for these two miRNAs in CRC;Moreover EZH2 was upregulated and inversely correlated with miR-26a expression in the osteosarcoma tissues; Thus for the first time we provide convincing evidence that downregulation of miR-26a is associated with tumor aggressiveness and tumor metastasis and miR-26a inhibits cell migration and invasion by targeting the EZH2 gene in osteosarcoma;Through down-regulation of EZH2 expression and up-regulation of E-cadherin expression miR-26a inhibited the EMT process in vitro and in vivo; Luciferase reporter assay showed that miR-26a directly interacted with EZH2 messenger RNA mRNA; Furthermore the expression of miR-26a was positively correlated with E-cadherin expression and inversely correlated with EZH2 expression in human HCC tissue; miR-26a inhibited the EMT process in HCC by down-regulating EZH2 expression;Previously EZH2 was shown to be regulated by miR-26a at the translational levels in lymphomas;miR 26a promoted by interferon alpha inhibits hepatocellular carcinoma proliferation and migration by blocking EZH2; Here we report that the IFN-α-induced microRNA-26a miR-26a can inhibit HCC proliferation and invasion by suppressing enhancer of zeste homologue 2 EZH2 expression in tumor cells; It was shown that there was increased miR-26a accompanied with downregulated EZH2 expression in the HCC specimens and EZH2 mRNA levels were inversely correlated with miR-26a expression; In addition the miR-26a mimic transfection decreased the EZH2 expression level significantly in the transfected HepG2 cells and inhibited HepG2 cell proliferation and invasion effectively; Our results indicate that miR-26a exerts growth inhibition in HCC and that its inhibitory effect is mediated briefly by blocking EZH2 expression;miR-26a inhibition partly prevents the metformin viability effect and the PTEN and EZH2 expression reduction;We also found that reexpression of miR-26a by transfection led to decreased expression of EZH2 and EpCAM in pancreatic cancer cells;In the present study the influence of miR-26a and miR-138 on EZH2 and cellular function including the impact on the cell cycle regulating network was evaluated in PCa cells; The present findings suggest an anti-proliferative role for miR-26a and miR-138 in PCa by blocking the G1/S-phase transition independent of EZH2 but via a concerted inhibition of crucial cell cycle regulators;We propose the hypermethylation of miR-26a as an alternative pathway of ERG rearrangement-independent EZH2 activation;High miR 26a and low CDC2 levels associate with decreased EZH2 expression and with favorable outcome on tamoxifen in metastatic breast cancer; Main objective of the present study is to investigate miR-26a and miR-101 levels which both target EZH2 for their association with molecular pathways and with efficacy of tamoxifen as first-line monotherapy for metastatic breast cancer; Cell cycle regulation and CCNE1 and CDC2 were the only significant overlapping pathway and genes differentially expressed between tumors with high and low levels of miR-26a and EZH2 respectively; Cell cycle regulation is the only overlapping pathway linked to miR-26a and EZH2 levels; Low mRNA levels of EZH2 CCNE1 and CDC2 and high levels of miR-26a are associated with favorable outcome on tamoxifen	tumorigenesis;;;metastasis;cell migration;;;;;;;;	breast cancer;breast cancer;colorectal cancer;sarcoma;liver cancer;acute myeloid leukemia;liver cancer;breast cancer;pancreatic cancer;prostate cancer;prostate cancer;breast cancer
hsa-miR-30d-5p	EZH2	-0.920901858717441	3.50898334321668e-05	2.63566539246403	3.78349576722754e-27	miRNAWalker2_validate;miRTarBase	-0.419247056844577	5.65026988406957e-16	22399519	Down regulation of the miR 25 and miR 30d contributes to the development of anaplastic thyroid carcinoma targeting the polycomb protein EZH2; We report that miR-25 and miR-30d target the polycomb protein enhancer of zeste 2 EZH2 that has oncogenic activity and is drastically up-regulated in anaplastic thyroid carcinomas but not in the differentiated ones; The down-regulation of miR-25 and miR-30d could contribute to the process of thyroid cancer progression leading to the development of anaplastic carcinomas targeting EZH2 mRNA	progression	thyroid cancer
hsa-miR-320a	EZH2	-0.961144925954715	1.62478794429204e-08	2.63566539246403	3.78349576722754e-27	miRNAWalker2_validate	-0.33780915530801	9.87948089196379e-07		NA	NA	NA