miRNA	gene	miRNA_log2FC	miRNA_pvalue	gene_log2FC	gene_pvalue	interactions	correlation_beta	correlation_pvalue	PMID	evidence	outcome	cancer
hsa-miR-30d-5p	CASP3	-0.920901858717441	3.50898334321668e-05	0.749868979708077	8.30799302647668e-11	miRNAWalker2_validate;miRTarBase;miRNATAP	-0.173377620122409	2.06657661969359e-13		NA	NA	NA
hsa-miR-106a-5p	CCND1	1.3902608059488	6.07931522284525e-05	-0.295767629587253	0.255400743295204	MirTarget;miRNATAP	-0.247441760563832	4.58943715400631e-11		NA	NA	NA
hsa-miR-106b-5p	CCND1	1.47447672652218	1.32004094930462e-13	-0.295767629587253	0.255400743295204	miRNAWalker2_validate;miRTarBase;MirTarget;miRNATAP	-0.261384817974007	7.4979419817232e-06		NA	NA	NA
hsa-miR-15a-5p	CCND1	1.62575353599172	1.55312121019827e-19	-0.295767629587253	0.255400743295204	miRNAWalker2_validate;miRTarBase;MirTarget;miRNATAP	-0.199069637483131	0.0019294787514794	22922827	CCND1 has been found to be a target of miR-15a and miR-16-1 through analysis of complementary sequences between microRNAs and CCND1 mRNA; Moreover the transcription of CCND1 is suppressed by miR-15a and miR-16-1 via direct binding to the CCND1 3'-untranslated region 3'-UTR		sarcoma
hsa-miR-15b-5p	CCND1	-1.25935038177398	1.83460220856901e-12	-0.295767629587253	0.255400743295204	miRNAWalker2_validate;miRTarBase;MirTarget;miRNATAP	-0.303824360423629	3.25741318048184e-06		NA	NA	NA
hsa-miR-16-1-3p	CCND1	1.50034693398929	6.63958242991125e-10	-0.295767629587253	0.255400743295204	miRNAWalker2_validate;miRTarBase	-0.249107447749185	3.23141967346606e-05	22922827;18483394	CCND1 has been found to be a target of miR-15a and miR-16-1 through analysis of complementary sequences between microRNAs and CCND1 mRNA; Moreover the transcription of CCND1 is suppressed by miR-15a and miR-16-1 via direct binding to the CCND1 3'-untranslated region 3'-UTR;Truncation in CCND1 mRNA alters miR 16 1 regulation in mantle cell lymphoma; Furthermore we demonstrated that this truncation alters miR-16-1 binding sites and through the use of reporter constructs we were able to show that miR-16-1 regulates CCND1 mRNA expression; This study introduces the role of miR-16-1 in the regulation of CCND1 in MCL	;	sarcoma;lymphoma
hsa-miR-16-5p	CCND1	0.749619098384047	4.11649450706988e-06	-0.295767629587253	0.255400743295204	miRNAWalker2_validate;miRTarBase;MirTarget;miRNATAP	-0.371885624299403	3.21606546730418e-07	23991964;22922827;18483394	At the molecular level our results further revealed that cyclin D1 expression was negatively regulated by miR-16;CCND1 has been found to be a target of miR-15a and miR-16-1 through analysis of complementary sequences between microRNAs and CCND1 mRNA; Moreover the transcription of CCND1 is suppressed by miR-15a and miR-16-1 via direct binding to the CCND1 3'-untranslated region 3'-UTR;Truncation in CCND1 mRNA alters miR 16 1 regulation in mantle cell lymphoma; Furthermore we demonstrated that this truncation alters miR-16-1 binding sites and through the use of reporter constructs we were able to show that miR-16-1 regulates CCND1 mRNA expression; This study introduces the role of miR-16-1 in the regulation of CCND1 in MCL	;;	bladder cancer;sarcoma;lymphoma
hsa-miR-17-5p	CCND1	2.07078488653279	2.77403038572568e-19	-0.295767629587253	0.255400743295204	miRNAWalker2_validate;MirTarget;TargetScan;miRNATAP	-0.313758634258834	1.59321495552009e-10	26431674	Bioinformatics Prediction and In Vitro Analysis Revealed That miR 17 Targets Cyclin D1 mRNA in Triple Negative Breast Cancer Cells; In this study using bioinformatic analyses miR-17 was selected as it targets the 3'UTR of CCND1 gene with the highest score; After lentiviral transduction of miR-17 to the target cells gene expression analysis showed decreased expression of CCND1 gene		breast cancer
hsa-miR-193a-3p	CCND1	0.549173467360291	0.0319030569365466	-0.295767629587253	0.255400743295204	MirTarget;PITA;miRanda	-0.190950932146342	0.000161171890671323		NA	NA	NA
hsa-miR-193b-3p	CCND1	1.10444771306846	0.000822888533401377	-0.295767629587253	0.255400743295204	miRNAWalker2_validate;miRTarBase;MirTarget	-0.147999411883792	3.70620495015026e-05	27071318;20655737;20304954;21893020;26129688	MicroRNA 193b inhibits the proliferation migration and invasion of gastric cancer cells via targeting cyclin D1; Further mechanism study indicated that CCND1 was a direct target of miR-193b in GC;CCND1 and ETS1 were revealed to be regulated by miR-193b directly;MicroRNA 193b represses cell proliferation and regulates cyclin D1 in melanoma; Overexpression of miR-193b in Malme-3M cells down-regulated CCND1 mRNA and protein by > or = 50%; A luciferase reporter assay confirmed that miR-193b directly regulates CCND1 by binding to the 3'untranslated region of CCND1 mRNA; These studies indicate that miR-193b represses cell proliferation and regulates CCND1 expression and suggest that dysregulation of miR-193b may play an important role in melanoma development;In a previous study we reported that miR-193b represses cell proliferation and regulates cyclin D1 in melanoma cells suggesting that miR-193b could act as a tumor suppressor;Epigenetically altered miR 193b targets cyclin D1 in prostate cancer; It has been suggested that miR-193b targets cyclin D1 in several malignancies; Here our aim was to determine if miR-193b targets cyclin D1 in prostate cancer; Furthermore the PC cell lines 22Rv1 and VCaP which express low levels of miR-193b and high levels of CCND1 showed significant growth retardation when treated with a CDK4/6 inhibitor; In contrast the inhibitor had no effect on the growth of PC-3 and DU145 cells with high miR-193b and low CCND1 expression; Taken together our data demonstrate that miR-193b targets cyclin D1 in prostate cancer	;;;;	gastric cancer;liver cancer;melanoma;melanoma;prostate cancer
hsa-miR-19a-3p	CCND1	2.11776595911517	7.07663078397156e-10	-0.295767629587253	0.255400743295204	miRNAWalker2_validate;miRTarBase;miRNATAP	-0.21539529985992	9.86203433305448e-08	25985117	Moreover miR-19a might play inhibitory roles in HCC malignancy via regulating Cyclin D1 expression		liver cancer
hsa-miR-19b-1-5p	CCND1	1.71217036351784	3.28561659177495e-12	-0.295767629587253	0.255400743295204	miRNAWalker2_validate;miRTarBase	-0.301713494105536	2.89182846291565e-08		NA	NA	NA
hsa-miR-20a-5p	CCND1	2.64649625616975	5.1469418982085e-27	-0.295767629587253	0.255400743295204	miRNAWalker2_validate;miRTarBase;MirTarget;miRNATAP	-0.237160136465301	1.84669386058676e-07		NA	NA	NA
hsa-miR-20b-5p	CCND1	1.35770573270947	0.00260808530013016	-0.295767629587253	0.255400743295204	MirTarget;miRNATAP	-0.179107595068828	5.65966117118738e-11		NA	NA	NA
hsa-miR-365a-3p	CCND1	0.0132777124336201	0.953597412537431	-0.295767629587253	0.255400743295204	miRNAWalker2_validate;miRTarBase	-0.193166924738263	0.000234492957903034		NA	NA	NA
hsa-miR-374b-5p	CCND1	0.474691035780475	0.0109217471394203	-0.295767629587253	0.255400743295204	miRNAWalker2_validate;MirTarget	-0.26116225100222	0.00011561978488339		NA	NA	NA
hsa-miR-93-5p	CCND1	1.50844106515467	1.83836866996875e-12	-0.295767629587253	0.255400743295204	miRNAWalker2_validate;MirTarget;miRNATAP	-0.320397820083252	2.84014735439528e-09		NA	NA	NA
hsa-miR-106b-5p	CCND2	1.47447672652218	1.32004094930462e-13	-1.64140990579885	1.49666938681079e-12	miRNAWalker2_validate;miRTarBase;miRNATAP	-0.383655587509124	2.65429916887189e-13		NA	NA	NA
hsa-miR-141-3p	CCND2	3.36993755486106	5.42939251147195e-32	-1.64140990579885	1.49666938681079e-12	MirTarget;TargetScan	-0.239914655059016	6.4654039095017e-12		NA	NA	NA
hsa-miR-15a-5p	CCND2	1.62575353599172	1.55312121019827e-19	-1.64140990579885	1.49666938681079e-12	miRNAWalker2_validate;miRTarBase;miRNATAP	-0.158338209854594	0.00711668272045409		NA	NA	NA
hsa-miR-16-5p	CCND2	0.749619098384047	4.11649450706988e-06	-1.64140990579885	1.49666938681079e-12	miRNAWalker2_validate;miRNATAP	-0.135197503151631	0.0448488951166271		NA	NA	NA
hsa-miR-17-5p	CCND2	2.07078488653279	2.77403038572568e-19	-1.64140990579885	1.49666938681079e-12	miRNAWalker2_validate;miRTarBase;TargetScan;miRNATAP	-0.365048259055278	1.61934056872758e-16		NA	NA	NA
hsa-miR-182-5p	CCND2	3.21839823004635	5.13049145201115e-39	-1.64140990579885	1.49666938681079e-12	miRNAWalker2_validate;miRTarBase;miRNATAP	-0.373145719566719	1.32597677460149e-21		NA	NA	NA
hsa-miR-185-5p	CCND2	1.14291034858482	2.95777119743491e-13	-1.64140990579885	1.49666938681079e-12	MirTarget;miRNATAP	-0.23940712387784	0.000484175543966546		NA	NA	NA
hsa-miR-186-5p	CCND2	0.852175445703945	6.88885738584309e-10	-1.64140990579885	1.49666938681079e-12	mirMAP;miRNATAP	-0.357370184588874	5.14493635358813e-06		NA	NA	NA
hsa-miR-19a-3p	CCND2	2.11776595911517	7.07663078397156e-10	-1.64140990579885	1.49666938681079e-12	MirTarget;miRNATAP	-0.167455065978335	6.56621464464812e-06		NA	NA	NA
hsa-miR-19b-3p	CCND2	2.10868505662119	5.40846613768389e-17	-1.64140990579885	1.49666938681079e-12	miRNAWalker2_validate;MirTarget;miRNATAP	-0.19157786848984	1.39328108679414e-05		NA	NA	NA
hsa-miR-20a-5p	CCND2	2.64649625616975	5.1469418982085e-27	-1.64140990579885	1.49666938681079e-12	miRNAWalker2_validate;miRTarBase;miRNATAP	-0.28367508352758	5.6750334332974e-12		NA	NA	NA
hsa-miR-320b	CCND2	0.226640952564488	0.378818692487242	-1.64140990579885	1.49666938681079e-12	mirMAP;miRNATAP	-0.123605256651271	0.00373003525561283		NA	NA	NA
hsa-miR-450b-5p	CCND2	1.69248953402469	1.96052058003353e-07	-1.64140990579885	1.49666938681079e-12	MirTarget;PITA;miRNATAP	-0.145422700655101	8.53356735526403e-05		NA	NA	NA
hsa-miR-501-5p	CCND2	0.411357595674671	0.10435288464149	-1.64140990579885	1.49666938681079e-12	PITA;mirMAP;miRNATAP	-0.144149908130612	0.000856140982438327		NA	NA	NA
hsa-miR-590-3p	CCND2	0.83851360565783	0.00129224433453587	-1.64140990579885	1.49666938681079e-12	miRanda;mirMAP	-0.133052154455084	0.00820830741469702		NA	NA	NA
hsa-miR-96-5p	CCND2	3.0381097138467	4.40362891630201e-24	-1.64140990579885	1.49666938681079e-12	TargetScan;miRNATAP	-0.357833634781266	1.13611538125112e-20		NA	NA	NA
hsa-miR-421	CCND3	0.170525317701774	0.535277026680289	-0.858556164090156	9.93688486289821e-06	PITA;miRanda	-0.120402813664522	0.000730915299268324		NA	NA	NA
hsa-miR-195-5p	CCNE1	-1.01577502605386	4.80814718341729e-05	2.99717740665025	1.61069658019784e-19	miRNAWalker2_validate;MirTarget;miRNATAP	-0.51804360034979	1.42698078497522e-15	24402230	Furthermore through qPCR and western blot assays we showed that overexpression of miR-195-5p reduced CCNE1 mRNA and protein levels respectively		breast cancer
hsa-miR-26a-5p	CCNE1	-0.126411409001078	0.440028840408711	2.99717740665025	1.61069658019784e-19	miRNAWalker2_validate;miRTarBase;miRNATAP	-0.695101497950461	4.5037170303388e-13	22094936	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; Low mRNA levels of EZH2 CCNE1 and CDC2 and high levels of miR-26a are associated with favorable outcome on tamoxifen		breast cancer
hsa-miR-497-5p	CCNE1	-0.0546347378264729	0.786205564901684	2.99717740665025	1.61069658019784e-19	MirTarget;miRNATAP	-0.495681038343954	2.32850749141189e-10	25909221;24112607;24909281	The effect of simultaneous overexpression of miR-497 and miR-34a on the inhibition of cell proliferation colony formation and tumor growth and the downregulation of cyclin E1 was stronger than the effect of each miRNA alone; The synergistic actions of miR-497 and miR-34a partly correlated with cyclin E1 levels; These results indicate cyclin E1 is downregulated by both miR-497 and miR-34a which synergistically retard the growth of human lung cancer cells;Western blot assays confirmed that overexpression of miR-497 reduced cyclin E1 protein levels; Inhibited cellular growth suppressed cellular migration and invasion and G1 cell cycle arrest were observed upon overexpression of miR-497 in cells possibly by targeting cyclin E1;miR 497 suppresses proliferation of human cervical carcinoma HeLa cells by targeting cyclin E1; Furthermore the target effect of miR-497 on the CCNE1 was identified by dual-luciferase reporter assay system qRT-PCR and Western blotting; Over-expressed miR-497 in HeLa cells could suppress cell proliferation by targeting CCNE1	;;	lung cancer;breast cancer;cervical and endocervical cancer
hsa-miR-26a-5p	CCNE2	-0.126411409001078	0.440028840408711	2.14869777933212	3.82193505863706e-13	miRNAWalker2_validate;miRTarBase;miRNATAP	-0.509665959363437	2.11729025570925e-09	24116110;21901171	The loss of miR 26a mediated post transcriptional regulation of cyclin E2 in pancreatic cancer cell proliferation and decreased patient survival; The in vitro and in vivo assays showed that overexpression of miR-26a resulted in cell cycle arrest inhibited cell proliferation and decreased tumor growth which was associated with cyclin E2 downregulation;We also show that enforced expression of miR-26a in AML cells is able to inhibit cell cycle progression by downregulating cyclin E2 expression	poor survival;progression	pancreatic cancer;acute myeloid leukemia
hsa-miR-30b-5p	CCNE2	0.358144314839612	0.138026229059594	2.14869777933212	3.82193505863706e-13	miRNAWalker2_validate;miRTarBase	-0.201650464117881	0.000503320898048745	22384020	A luciferase-based reporter assay demonstrated that miR-30b post-transcriptionally reduced 27% p = 0.005 of the gene expression by interacting with two binding sites in the 3'-UTR of CCNE2; The upregulation of miR-30b by trastuzumab may play a biological role in trastuzumab-induced cell growth inhibition by targeting CCNE2		breast cancer
hsa-miR-34a-5p	CCNE2	1.40588612517769	8.60097477768592e-12	2.14869777933212	3.82193505863706e-13	miRNAWalker2_validate;miRTarBase;miRNATAP	-0.195460410714665	0.00336778531948037		NA	NA	NA
hsa-miR-34c-5p	CCNE2	-1.00125440032112	0.0724432896090357	2.14869777933212	3.82193505863706e-13	miRNAWalker2_validate;miRTarBase;PITA;miRanda;miRNATAP	-0.107375543427311	4.3380723232889e-05		NA	NA	NA
hsa-miR-23a-3p	CCNG1	0.111958289789488	0.393086414480463	-0.381998946658134	0.021474550007251	MirTarget;miRNATAP	-0.183198674467916	0.00202799417869928		NA	NA	NA
hsa-miR-27a-3p	CCNG1	0.433402568013802	0.00737164631768323	-0.381998946658134	0.021474550007251	MirTarget;miRNATAP	-0.25375430158064	7.1666208486228e-08		NA	NA	NA
hsa-miR-27b-3p	CCNG1	0.236438984240408	0.12263510345883	-0.381998946658134	0.021474550007251	MirTarget;miRNATAP	-0.172140886867638	0.000639941826798135	26623719	Moreover miR-27b directly targets the 3' untranslated regions 3'-UTRs of CCNG1 a well-known negative regulator of P53 stability; Interestingly miR-27b up-regulation leads to increased miR-508-5p expression and this phenomenon is mediated by CCNG1 and P53		gastric cancer
hsa-miR-96-5p	CCNG1	3.0381097138467	4.40362891630201e-24	-0.381998946658134	0.021474550007251	MirTarget;TargetScan	-0.125986304075834	5.6639500582943e-06		NA	NA	NA
hsa-miR-664a-3p	CCNG2	0.443077463053857	0.0214248925850984	0.220278413829613	0.10547582961774	MirTarget;mirMAP	-0.160018466299354	7.23956577877032e-07		NA	NA	NA
hsa-miR-145-5p	CDK4	-1.34926078156437	2.63526538800669e-07	0.737437814725925	6.46735685355202e-06	miRNAWalker2_validate;miRTarBase	-0.151032894863878	9.5680433026529e-08	21092188	Furthermore we found that CDK4 was regulated by miR-145 in cell cycle control		lung squamous cell cancer
hsa-miR-195-5p	CDK4	-1.01577502605386	4.80814718341729e-05	0.737437814725925	6.46735685355202e-06	miRNAWalker2_validate;miRTarBase	-0.113117227761123	0.000369485847021713		NA	NA	NA
hsa-miR-24-3p	CDK4	-0.0357874587555003	0.785865078836504	0.737437814725925	6.46735685355202e-06	miRNAWalker2_validate;miRTarBase	-0.116959746098431	0.0466601645219138		NA	NA	NA
hsa-miR-141-3p	CDK6	3.36993755486106	5.42939251147195e-32	-0.634679756888932	0.0174689602657709	TargetScan;miRNATAP	-0.160612180698081	5.76268904101641e-05		NA	NA	NA
hsa-miR-21-5p	CDK6	4.38165933891779	1.52536633902505e-92	-0.634679756888932	0.0174689602657709	miRNAWalker2_validate;mirMAP	-0.148024006269382	0.00157509032784336		NA	NA	NA
hsa-miR-29b-3p	CDK6	3.10527711861309	3.01242507282711e-32	-0.634679756888932	0.0174689602657709	miRNAWalker2_validate;miRTarBase;miRNATAP	-0.177579122887668	4.47727335928492e-05	23591808;23245396;25472644;26180082;27230400;20086245	Here we have identified the oncogene cyclin-dependent protein kinase 6 CDK6 as a direct target of miR-29b in lung cancer;The IFN-γ-induced G1-arrest of melanoma cells involves down-regulation of CDK6 which we proved to be a direct target of miR-29 in these cells;Moreover miR-29b inhibited the expression of MCL1 and CDK6;Knockdown of NTSR1 increased the expression of miR-29b-1 and miR-129-3p which were responsible for the decreased CDK6 expression;MiR 29b suppresses the proliferation and migration of osteosarcoma cells by targeting CDK6; In this study we investigated the role of miR-29b as a novel regulator of CDK6 using bioinformatics methods; We demonstrated that CDK6 can be downregulated by miR-29b via binding to the 3'-UTR region in osteosarcoma cells; Furthermore we identified an inverse correlation between miR-29b and CDK6 protein levels in osteosarcoma tissues; The results revealed that miR-29b acts as a tumor suppressor of osteosarcoma by targeting CDK6 in the proliferation and migration processes;microRNA expression profile and identification of miR 29 as a prognostic marker and pathogenetic factor by targeting CDK6 in mantle cell lymphoma; Furthermore we demonstrate miR-29 inhibition of CDK6 protein and mRNA levels by direct binding to 3'-untranslated region; Inverse correlation between miR-29 and CDK6 was observed in MCL	;;;;;	lung cancer;melanoma;colorectal cancer;glioblastoma;sarcoma;lymphoma
hsa-miR-34a-5p	CDK6	1.40588612517769	8.60097477768592e-12	-0.634679756888932	0.0174689602657709	miRNAWalker2_validate;miRTarBase;miRNATAP	-0.243763697376835	2.99239665927089e-05	26104764;21702042	The expression of microRNA 34a is inversely correlated with c MET and CDK6 and has a prognostic significance in lung adenocarcinoma patients; We found significant inverse correlations between miR-34a and c-MET R = -0.316 P = 0.028 and CDK6 expression R = -0.4582 P = 0.004;Molecular analyses identified Cdk6 and sirtuin SIRT-1 as being targeted by miR-34a in MI-TCC cells however inhibition of Cdk6 and SIRT-1 was not as effective as pre-miR-34a in mediating chemosensitization	;	lung cancer;bladder cancer
hsa-miR-429	CDK6	2.3794516574089	1.72813419703734e-13	-0.634679756888932	0.0174689602657709	mirMAP;miRNATAP	-0.15019667316567	0.000181432042876184		NA	NA	NA
hsa-miR-106b-5p	CDKN1A	1.47447672652218	1.32004094930462e-13	-0.989660104023605	3.33169106596478e-07	miRNAWalker2_validate;miRTarBase;MirTarget;miRNATAP	-0.227776235142808	2.11586866823657e-07		NA	NA	NA
hsa-miR-17-5p	CDKN1A	2.07078488653279	2.77403038572568e-19	-0.989660104023605	3.33169106596478e-07	miRNAWalker2_validate;miRTarBase;MirTarget;TargetScan;miRNATAP	-0.155626227970113	3.32801748379634e-05	26482648;24989082	The low expressions of miR-17 and miR-92 families can maintain cisplatin resistance through the regulation of CDKN1A and RAD21;According to PicTar and Miranda algorithms which predicted CDKN1A p21 as a putative target of miR-17 a luciferase assay was performed and revealed that miR-17 directly targets the 3'-UTR of p21 mRNA	drug resistance;	lung squamous cell cancer;sarcoma
hsa-miR-20a-5p	CDKN1A	2.64649625616975	5.1469418982085e-27	-0.989660104023605	3.33169106596478e-07	miRNAWalker2_validate;miRTarBase;MirTarget;miRNATAP	-0.137674450234877	6.74026700667366e-05	26012475	Using the poorly tumorigenic and TGF-β-sensitive FET cell line that expresses low miR-20a levels we first confirmed that miR-20a downmodulated CDKN1A expression both at mRNA and protein level through direct binding to its 3'-UTR; Moreover besides modulating CDKN1A miR-20a blocked TGF-β-induced transactivation of its promoter without affecting the post-receptor activation of Smad3/4 effectors directly; Finally miR-20a abrogated the TGF-β-mediated c-Myc repression a direct inhibitor of the CDKN1A promoter activation most likely by reducing the expression of specific MYC-regulating genes from the Smad/E2F-based core repressor complex		colon cancer
hsa-miR-28-5p	CDKN1A	1.19639196514745	4.59365801666536e-18	-0.989660104023605	3.33169106596478e-07	miRNAWalker2_validate;miRTarBase;MirTarget;miRanda;miRNATAP	-0.202389894871562	0.0015056884290614		NA	NA	NA
hsa-miR-93-5p	CDKN1A	1.50844106515467	1.83836866996875e-12	-0.989660104023605	3.33169106596478e-07	miRNAWalker2_validate;miRTarBase;MirTarget;miRNATAP	-0.165683989353739	5.62354734150849e-05	25633810	MicroRNA 93 activates c Met/PI3K/Akt pathway activity in hepatocellular carcinoma by directly inhibiting PTEN and CDKN1A; We confirmed that miR-93 directly bound with the 3' untranslated regions of the tumor-suppressor genes PTEN and CDKN1A respectivelyand inhibited their expression; We concluded that miR-93 stimulated cell proliferation migration and invasion through the oncogenic c-Met/PI3K/Akt pathway and also inhibited apoptosis by directly inhibiting PTEN and CDKN1A expression in human HCC		liver cancer
hsa-miR-96-5p	CDKN1A	3.0381097138467	4.40362891630201e-24	-0.989660104023605	3.33169106596478e-07	miRNAWalker2_validate;miRTarBase	-0.146610096725374	7.80340952179366e-06	26582573	Upregulation of microRNA 96 and its oncogenic functions by targeting CDKN1A in bladder cancer; Bioinformatics prediction combined with luciferase reporter assay were used to verify whether the cyclin-dependent kinase inhibitor CDKN1A was a potential target gene of miR-96; According to the data of miRTarBase CDKN1A might be a candidate target gene of miR-96; In addition luciferase reporter and Western blot assays respectively demonstrated that miR-96 could bind to the putative seed region in CDKN1A mRNA 3'UTR and significantly reduce the expression level of CDKN1A protein; Moreover we found that the inhibition of miR-96 expression remarkably decreased cell proliferation and promoted cell apoptosis of BC cell lines which was consistent with the findings observed following the introduction of CDKN1A cDNA without 3'UTR restored miR-96; Upregulation of miR-96 may contribute to aggressive malignancy partly through suppressing CDKN1A protein expression in BC cells		bladder cancer
hsa-miR-98-5p	CDKN1A	1.170602085804	1.09900501665229e-08	-0.989660104023605	3.33169106596478e-07	miRNAWalker2_validate;MirTarget	-0.101157293449583	0.0239980027641424		NA	NA	NA
hsa-miR-195-5p	CHEK1	-1.01577502605386	4.80814718341729e-05	1.85259564745725	8.22396650402656e-14	MirTarget;miRNATAP	-0.345574150233039	7.39222165825211e-13	25840419	MiR 195 suppresses non small cell lung cancer by targeting CHEK1; We discovered that CHEK1 was a direct target of miR-195 which decreased CHEK1 expression in lung cancer cells		lung squamous cell cancer
hsa-miR-320a	CHEK1	-0.961144925954715	1.62478794429204e-08	1.85259564745725	8.22396650402656e-14	MirTarget;miRanda	-0.279842886792326	4.08338178278489e-05		NA	NA	NA
hsa-miR-497-5p	CHEK1	-0.0546347378264729	0.786205564901684	1.85259564745725	8.22396650402656e-14	MirTarget;miRNATAP	-0.487503389798205	7.93376609427637e-18	24464213	Checkpoint kinase 1 is negatively regulated by miR 497 in hepatocellular carcinoma; In silico analysis showed that CHEK1 was a candidate target of miR-497 which was previously found to be downregulated in HCC by us; To test whether miR-497 could bind to 3'untranslated region 3'UTR of CHEK1 luciferase reporter assay was conducted; The result revealed that miR-497 could bind to the 3'untranslated region 3'UTR of CHEK1 mRNA; Western blot showed that ectopic expression of miR-497 suppressed the CHEK1 expression and inhibition of miR-497 led to significant upregulation of CHEK1; Finally miR-497 expression was measured in the same 30 HCC samples and the correlation between miR-497 and CHEK1 was analyzed; The results indicated that miR-497 was downregulated in HCC and had a significant negative correlation with CHEK1; Taken together these results demonstrated that CHEK1 was negatively regulated by miR-497 and the overexpressed CHEK1 was resulted from the downregulated miR-497 in HCC which provided a potential molecular target for HCC therapy		liver cancer
hsa-miR-106a-5p	FAS	1.3902608059488	6.07931522284525e-05	-0.878746828084236	0.000340153420442741	miRNAWalker2_validate;miRTarBase	-0.274948885695996	7.27787651364869e-15	22431000;27142596	miR 106a is frequently upregulated in gastric cancer and inhibits the extrinsic apoptotic pathway by targeting FAS; Bioinformatic analysis combining with validation experiments identified FAS as a direct target of miR-106a; Moreover a significant inverse correlation was found between miR-106a and FAS expression not only in gastric cancer cell lines but also in gastric cancer specimens; Taken together these findings suggest that ectopicly overexpressed miR-106a may play an oncogenic role in gastric carcinogenesis and impair extrinsic apoptotic pathway through targeting FAS;Functional experiment ascertained that miR-106a interacted with FAS and mediated caspase3 pathway	tumorigenesis;	gastric cancer;gastric cancer
hsa-miR-324-3p	GADD45B	-0.0774700133118458	0.689226297032231	-1.592999067635	1.71286942854757e-12	MirTarget;miRNATAP	-0.153520773002313	0.00557801960543285		NA	NA	NA
hsa-miR-127-3p	GADD45G	-0.723429813065737	0.0192747925933947	0.558251242266569	0.0699587843678354	miRanda;miRNATAP	-0.177067134124427	0.000105410370152299		NA	NA	NA
hsa-miR-361-5p	IGF1	0.21454431962475	0.0800957579368424	-0.878839289406132	0.00545024687919024	PITA;mirMAP	-0.259580395383156	0.0330038273746438		NA	NA	NA
hsa-miR-450b-5p	IGF1	1.69248953402469	1.96052058003353e-07	-0.878839289406132	0.00545024687919024	MirTarget;PITA;mirMAP;miRNATAP	-0.155478745947113	0.00168638246971297		NA	NA	NA
hsa-miR-576-5p	IGF1	1.02693643167056	1.14846964470173e-06	-0.878839289406132	0.00545024687919024	PITA;mirMAP;miRNATAP	-0.319877018116458	2.70279102064343e-06		NA	NA	NA
hsa-miR-590-3p	IGF1	0.83851360565783	0.00129224433453587	-0.878839289406132	0.00545024687919024	MirTarget;miRanda;mirMAP;miRNATAP	-0.218208367579052	0.00112544995000528		NA	NA	NA
hsa-miR-374a-5p	IGFBP3	-0.197027254874826	0.298080902192861	1.34688121148136	3.19621778611777e-05	MirTarget;mirMAP	-0.199714191096732	0.0260582852002187		NA	NA	NA
hsa-let-7a-5p	MDM4	-1.37014061604018	3.11451492971224e-14	0.499766401450246	0.00108403645699481	MirTarget;TargetScan	-0.117171041955205	0.00217657953672176		NA	NA	NA
hsa-miR-361-5p	MDM4	0.21454431962475	0.0800957579368424	0.499766401450246	0.00108403645699481	miRanda;mirMAP	-0.155647576630015	0.00808853891753239		NA	NA	NA
hsa-miR-200b-3p	PMAIP1	1.55157578247391	4.83790020897188e-09	1.3465665248913	2.20137844697311e-05	MirTarget;TargetScan	-0.250424090680499	4.05232937169968e-06		NA	NA	NA
hsa-miR-200c-3p	PMAIP1	0.380533388300368	0.0842181838538353	1.3465665248913	2.20137844697311e-05	miRNAWalker2_validate;miRTarBase;MirTarget	-0.307134734629427	4.00785088372381e-06		NA	NA	NA
hsa-miR-15a-5p	PPM1D	1.62575353599172	1.55312121019827e-19	-0.842960797921556	1.98543788687206e-14	MirTarget;miRNATAP	-0.200928037013903	1.69503908604022e-13		NA	NA	NA
hsa-miR-29a-3p	PPM1D	0.101650412194573	0.573201097011668	-0.842960797921556	1.98543788687206e-14	miRNAWalker2_validate;miRTarBase;MirTarget;miRNATAP	-0.130558636750052	6.16474771580982e-06		NA	NA	NA
hsa-miR-29b-3p	PPM1D	3.10527711861309	3.01242507282711e-32	-0.842960797921556	1.98543788687206e-14	MirTarget;miRNATAP	-0.184744077269729	4.36507328030672e-26		NA	NA	NA
hsa-miR-103a-3p	PTEN	0.538497806383155	1.88134691850591e-05	-0.41901734874011	0.000137135697667474	miRNAWalker2_validate;miRTarBase	-0.178416761140974	1.0244122893712e-05	26511107;24828205	LncRNA GAS5 induces PTEN expression through inhibiting miR 103 in endometrial cancer cells; To investigate the expression of GAS5 PTEN and miR-103 RT-PCR was performed; Finally we found that miR-103 mimic could decrease the mRNA and protein levels of PTEN through luciferase reporter assay and western blotting and GAS5 plasmid may reverse this regulation effect in endometrial cancer cells; Through inhibiting the expression of miR-103 GAS5 significantly enhanced the expression of PTEN to promote cancer cell apoptosis and thus could be an important mediator in the pathogenesis of endometrial cancer;Our data collectively demonstrate that miR-103 is an oncogene miRNA that promotes colorectal cancer proliferation and migration through down-regulation of the tumor suppressor genes DICER and PTEN	;	endometrial cancer;colorectal cancer
hsa-miR-106b-5p	PTEN	1.47447672652218	1.32004094930462e-13	-0.41901734874011	0.000137135697667474	miRNAWalker2_validate;miRTarBase;miRNATAP	-0.104117444261304	2.59660457077114e-05	24842611;26238857;26722252	MicroRNA 106b in cancer associated fibroblasts from gastric cancer promotes cell migration and invasion by targeting PTEN;We further identified PTEN and p21 as novel direct targets of miR-106b by using target prediction algorithms and a luciferase assay; Overexpression of miR-106b reduced the expression of PTEN and p21 and increased the expression of p-AKT which is a downstream of PTEN; Restoring the expression of PTEN or p21 in stably miR-106b-overexpressed cells could rescue the effect of miR-106b on cell radioresistance; These observations illustrated that miR-106b could induce cell radioresistance by directly targeting PTEN and p21 this process was accompanied by tumour-initiating cell capacity enhancement which is universally confirmed to be associated with radioresistance;Cantharidin modulates the E2F1/MCM7 miR 106b 93/p21 PTEN signaling axis in MCF 7 breast cancer cells	cell migration;drug resistance;	gastric cancer;colorectal cancer;breast cancer
hsa-miR-130a-3p	PTEN	0.881660100597014	0.000158893668519248	-0.41901734874011	0.000137135697667474	MirTarget;miRNATAP	-0.101775551899915	2.13139066434031e-06	24490491;27062783;22614869;26837847;27040383;27035216;26043084	Down-regulated miR-130a did not affect cell proliferations but enhanced the sensitivity of the cells to cisplatin inhibited the expressions of MDR1 mRNA and P-gp and increased the expression of PTEN proteins; MiR-130a inhibitor can reverse the cisplatin resistance by upregulating the expression of PTEN proteins and down-regulating P-gp in A2780 cell lines;Platinum-resistant patients had significantly higher levels of expression of miR-130a and BCL-2 and lower level of PTEN than platinum-sensitive patients P < 0.05; MiR-130a may mediate the generation of platinum resistance in epithelial ovarian cancer through inhibiting PTEN to activate PI3K/AKT signaling pathway and increasing BCL-2 to inhibit tumor cell apoptosis;We found that miR-130a was upregulated in SKOV3/CIS compared to the parental SKOV3 cells and PTEN was predicted to be the potential target of miR-130a;The miR 130 family promotes cell migration and invasion in bladder cancer through FAK and Akt phosphorylation by regulating PTEN; In clinical bladder cancer specimens downregulation of PTEN was found to be closely correlated with miR-130 family expression levels;In addition by targeting PTEN 3' untranslated region miR-130a might increase cell growth and initiate protein kinase B AKT pathway activation;MicroRNA 130a promotes the metastasis and epithelial mesenchymal transition of osteosarcoma by targeting PTEN; MiR-130a exerted promoting effects on metastatic behavior and EMT of osteosarcoma cells through suppressing PTEN expression;This role of miR-130a may be achieved by regulating the MDR1 and PTEN gene expression	drug resistance;drug resistance;;cell migration;;metastasis;	ovarian cancer;ovarian cancer;ovarian cancer;bladder cancer;cervical and endocervical cancer;sarcoma;ovarian cancer
hsa-miR-130b-3p	PTEN	1.83046548750752	5.04753914574694e-13	-0.41901734874011	0.000137135697667474	MirTarget;miRNATAP	-0.109728666497463	7.00361581570123e-08	26837847;25637514	The miR 130 family promotes cell migration and invasion in bladder cancer through FAK and Akt phosphorylation by regulating PTEN; In clinical bladder cancer specimens downregulation of PTEN was found to be closely correlated with miR-130 family expression levels;MiR 130b plays an oncogenic role by repressing PTEN expression in esophageal squamous cell carcinoma cells; We confirmed that miR-130b interacted with the 3'-untranslated region of PTEN and that an increase in the expression level of miR-130b negatively affected the protein level of PTEN; However the dysregulation of miR-130b had no obvious impact on PTEN mRNA; As Akt is a downstream effector of PTEN we explored if miR-130b affected Akt expression and found that miR-130b indirectly regulated the level of phosphorylated Akt while total Akt protein remained unchanged; The results indicate that miR-130b plays an oncogenic role in ESCC cells by repressing PTEN expression and Akt phosphorylation which would be helpful in developing miRNA-based treatments for ESCC	cell migration;	bladder cancer;esophageal cancer
hsa-miR-141-3p	PTEN	3.36993755486106	5.42939251147195e-32	-0.41901734874011	0.000137135697667474	miRNAWalker2_validate;miRTarBase;TargetScan;miRNATAP	-0.103983871313954	1.43928589517751e-10	27644195;24742567	Involvement of microRNA 141 3p in 5 fluorouracil and oxaliplatin chemo resistance in esophageal cancer cells via regulation of PTEN; Western blot exhibited altered protein levels of PTEN Akt and PI3k with miR-141-3p inhibitor; An inverse correlation between PTEN expression and miR-141-3p expression was also observed in tissue samples; Our study demonstrated that miR-141-3p contributed to an acquired chemo-resistance through PTEN modulation both in vitro and in vivo;PTEN might be a potential target of miR-141 and miR-200a in endometrial carcinogenesis	drug resistance;tumorigenesis	esophageal cancer;endometrial cancer
hsa-miR-148b-3p	PTEN	0.483970528590224	0.0026495409465901	-0.41901734874011	0.000137135697667474	MirTarget;miRNATAP	-0.130520184239271	3.47762829311644e-05		NA	NA	NA
hsa-miR-17-5p	PTEN	2.07078488653279	2.77403038572568e-19	-0.41901734874011	0.000137135697667474	miRNAWalker2_validate;miRTarBase;TargetScan;miRNATAP	-0.187397757344705	2.72047461827111e-20	27400681;23391506;23133552;26629823;24462867;26318586;26215320;25634356;26500892;24912422;23418359	GFRα2 prompts cell growth and chemoresistance through down regulating tumor suppressor gene PTEN via Mir 17 5p in pancreatic cancer; Mechanically we discovered that high GFRα2 expression level leads to PTEN inactivation via enhancing Mir-17-5p level;We found that these phenotypes were the results of miR-17 targeting PTEN;PTEN mRNA correlated inversely with miR-92a and members of the miR-17 and miR-130/301 families;We hypothesized that knocking down the oncogenic microRNA oncomiR miR-17-5p might restore the expression levels of PDCD4 and PTEN tumor suppressor proteins illustrating a route to oligonucleotide therapy of TNBC; Contrary to conventional wisdom antisense knockdown of oncomiR miR-17-5p guide strand reduced PDCD4 and PTEN proteins by 1.8±0.3 fold in human TNBC cells instead of raising them; Bioinformatics analysis and folding energy calculations revealed that mRNA targets of miR-17-5p guide strand such as PDCD4 and PTEN could also be regulated by miR-17-3p passenger strand;miR 17 inhibitor suppressed osteosarcoma tumor growth and metastasis via increasing PTEN expression; Expression of miR-17 was negatively correlated with PTEN in OS tissues;Resveratrol and pterostilbene epigenetically restore PTEN expression by targeting oncomiRs of the miR 17 family in prostate cancer; Further pterostilbene through downregulation of miR-17-5p and miR-106a-5p expression both in tumors and systemic circulation rescued PTEN mRNA and protein levels leading to reduced tumor growth in vivo;In addition ERβ expression significantly increased in calycosin-treated HCT-116 cells followed by a decrease of miR-17 and up-regulation of PTEN; Our results indicate that calycosin has an inhibitory effect on CRC which might be obtained by ERβ-mediated regulation of miR-17 and PTEN expression;The High Expression of the microRNA 17 92 Cluster and its Paralogs and the Downregulation of the Target Gene PTEN Is Associated with Primary Cutaneous B Cell Lymphoma Progression;MicroRNA 17 5p induces drug resistance and invasion of ovarian carcinoma cells by targeting PTEN signaling; miR-17-5p activates AKT by downregulation of PTEN in ovarian cancer cells;MicroRNA 17 5p promotes chemotherapeutic drug resistance and tumour metastasis of colorectal cancer by repressing PTEN expression; We found that PTEN was a target of miR-17-5p in the colon cancer cells and their context-specific interactions were responsible for multiple drug-resistance; Chemotherapy was found to increase the expression levels of miR-17-5p which further repressed PTEN levels contributing to the development of chemo-resistance; MiR-17-5p is a predictive factor for chemotherapy response and a prognostic factor for overall survival in CRC which is due to its regulation of PTEN expression;The mature miR-17-5p exerted this function by repressing the expression of PTEN	drug resistance;;;;metastasis;;;progression;drug resistance;metastasis;drug resistance;poor survival;	pancreatic cancer;glioblastoma;sarcoma;breast cancer;sarcoma;prostate cancer;colorectal cancer;B cell lymphoma;ovarian cancer;colorectal cancer;liver cancer
hsa-miR-186-5p	PTEN	0.852175445703945	6.88885738584309e-10	-0.41901734874011	0.000137135697667474	mirMAP;miRNATAP	-0.18571264902072	2.84306242795631e-07		NA	NA	NA
hsa-miR-18a-5p	PTEN	1.37435209536521	9.2173853686829e-06	-0.41901734874011	0.000137135697667474	miRNAWalker2_validate;miRTarBase	-0.141101959733646	1.18775251717657e-16	24681249;27291152	However higher levels of the miR-17~92 cluster switched from PTEN to oncogenes including Ctnnb1 β-catenin via miR-18a which resulted in inhibition of tumor growth and metastasis;miR 18a promotes cell proliferation of esophageal squamous cell carcinoma cells by increasing cylin D1 via regulating PTEN PI3K AKT mTOR signaling axis	metastasis;	colon cancer;esophageal cancer
hsa-miR-193a-3p	PTEN	0.549173467360291	0.0319030569365466	-0.41901734874011	0.000137135697667474	PITA;miRanda	-0.100107289825292	2.74866825496953e-06	26753960;23223432	Downregulation of microRNA 193 3p inhibits tumor proliferation migration and chemoresistance in human gastric cancer by regulating PTEN gene;Our study identifies miR-193a and PTEN as targets for AML1/ETO and provides evidence that links the epigenetic silencing of tumor suppressor genes miR-193a and PTEN to differentiation block of myeloid precursors	drug resistance;differentiation	gastric cancer;acute myeloid leukemia
hsa-miR-19a-3p	PTEN	2.11776595911517	7.07663078397156e-10	-0.41901734874011	0.000137135697667474	miRNAWalker2_validate;miRTarBase;MirTarget;miRNATAP	-0.152449210349358	4.83140828337759e-20	26098000;27289489;27445062;24831732;21853360;24681249;25107371	Moreover siRNA-mediated knockdown of PTEN a target of miR-19 also resulted in EMT migration and invasion of A549 and HCC827 cells suggesting that PTEN is involved in miR-19-induced EMT migration and invasion of lung cancer cells;Transfection of miR-19a and -19b mimics reversed the up-regulations of IGF2R and PTEN gene expression and abrogated the GSE induced anti-proliferative response;The target genes of miR-19a such as ABCA1 and PTEN that had been suppressed by miR recovered their expression through CAP treatment;Meanwhile BPA-induced upregulation of oncogenic miR-19a and miR-19b and the dysregulated expression of miR-19-related downstream proteins including PTEN p-AKT p-MDM2 p53 and proliferating cell nuclear antigen were reversed by curcumin;Regulation of miR 19 to breast cancer chemoresistance through targeting PTEN; Expression levels of miR-19 in MDR cells were inversely consistent with those of PTEN; Our findings demonstrate for the first time involvement of miR-19 in multidrug resistance through modulation of PTEN and suggest that miR-19 may be a potential target for preventing and reversing MDR in tumor cells;miR-19 in the context of the miR-17~92 cluster at medium levels promoted tumor metastasis through induction of Wnt/β-catenin-mediated epithelial-mesenchymal transition by targeting to the tumor-suppressor gene PTEN;The target of miR-19a was identified by western blot and whether its regulatory role depends on its target was improved by a rescue experiment with miR-19a mimic and PTEN expression plasmid; Meanwhile gain or loss of function of miR-19a demonstrated that miR-19a can promote cell growth of bladder cancer cells and the further mechanism studies indicated that its oncogenic role was dependent on targeting PTEN; The oncogenic role of miR19a in bladder cancer was dependent on targeting PTEN	;drug resistance;;;drug resistance;metastasis;	lung cancer;lung cancer;breast cancer;breast cancer;breast cancer;colon cancer;bladder cancer
hsa-miR-19b-3p	PTEN	2.10868505662119	5.40846613768389e-17	-0.41901734874011	0.000137135697667474	miRNAWalker2_validate;miRTarBase;MirTarget;miRNATAP	-0.144424393781319	5.95919159731141e-13	26098000;24831732;21853360;24681249	Moreover siRNA-mediated knockdown of PTEN a target of miR-19 also resulted in EMT migration and invasion of A549 and HCC827 cells suggesting that PTEN is involved in miR-19-induced EMT migration and invasion of lung cancer cells;Meanwhile BPA-induced upregulation of oncogenic miR-19a and miR-19b and the dysregulated expression of miR-19-related downstream proteins including PTEN p-AKT p-MDM2 p53 and proliferating cell nuclear antigen were reversed by curcumin;Regulation of miR 19 to breast cancer chemoresistance through targeting PTEN; Expression levels of miR-19 in MDR cells were inversely consistent with those of PTEN; Our findings demonstrate for the first time involvement of miR-19 in multidrug resistance through modulation of PTEN and suggest that miR-19 may be a potential target for preventing and reversing MDR in tumor cells;miR-19 in the context of the miR-17~92 cluster at medium levels promoted tumor metastasis through induction of Wnt/β-catenin-mediated epithelial-mesenchymal transition by targeting to the tumor-suppressor gene PTEN	;;drug resistance;metastasis	lung cancer;breast cancer;breast cancer;colon cancer
hsa-miR-20a-5p	PTEN	2.64649625616975	5.1469418982085e-27	-0.41901734874011	0.000137135697667474	miRNAWalker2_validate;miRTarBase;miRNATAP	-0.161121765339806	1.05381764637456e-17	26031366	The expression of miR-20a and PTEN were detected in HCC cell lines and paired primary tissues by quantitative real-time polymerase chain reaction; MiR-20a levels were increased in HCC cell lines and tissues whereas PTEN was inversely correlated with it; PTEN was identified as a direct functional target of miR-20a for the induction of radioresistance	drug resistance	liver cancer
hsa-miR-25-3p	PTEN	0.361927330834176	0.0163670566170988	-0.41901734874011	0.000137135697667474	miRTarBase;MirTarget;miRNATAP	-0.11968562938759	0.000411956693911945		NA	NA	NA
hsa-miR-26b-5p	PTEN	0.72362441215247	4.7794659748036e-05	-0.41901734874011	0.000137135697667474	MirTarget;miRNATAP	-0.101786450251327	0.000339227897329926	26068649	Down regulation of microRNA 26b modulates non small cell lung cancer cells chemoresistance and migration through the association of PTEN; It indicates that miR-26b may regulate NSCLC migration and chemosensitivity through the regulation of PTEN	drug resistance	lung squamous cell cancer
hsa-miR-301a-3p	PTEN	2.70198002906399	1.56420889710984e-14	-0.41901734874011	0.000137135697667474	MirTarget;miRNATAP	-0.136185588556865	5.91738747356386e-16	24315818;26846737	Upregulated microRNA 301a in breast cancer promotes tumor metastasis by targeting PTEN and activating Wnt/β catenin signaling; Furthermore miR-301a directly targeted and suppressed PTEN one negative regulator of the Wnt/β-catenin signaling cascade; These results demonstrate that miR-301a maintains constitutively activated Wnt/β-catenin signaling by directly targeting PTEN which promotes breast cancer invasion and metastasis;MicroRNA 301a promotes cell proliferation via PTEN targeting in Ewing's sarcoma cells; Our results demonstrated the novel mechanism controlling PTEN expression via miR-301a in ES cells	metastasis;	breast cancer;sarcoma
hsa-miR-454-3p	PTEN	1.49453641052169	4.46235742871434e-09	-0.41901734874011	0.000137135697667474	MirTarget;miRNATAP	-0.207669245917415	3.06891122776166e-20	26296312;27261580	MicroRNA 454 functions as an oncogene by regulating PTEN in uveal melanoma; Furthermore we identified PTEN as a direct target of miR-454; Our data revealed that ectopic expression of PTEN restored the effects of miR-454 on cell proliferation and invasion in uveal melanoma cells;MiR 454 promotes the progression of human non small cell lung cancer and directly targets PTEN; At last the potential regulatory function of miR-454 on PTEN expression was confirmed; Further PTEN was confirmed as a direct target of miR-454 by using Luciferase Reporter Assay	;progression	melanoma;lung squamous cell cancer
hsa-miR-92a-3p	PTEN	-0.136362762339122	0.493412263619364	-0.41901734874011	0.000137135697667474	MirTarget;miRNATAP	-0.123586887613975	1.14670739856895e-06	26432332;25515201;24137349;23546593;23133552;24026406	Downregulation of PTEN could mimic the same effects of miR-92a mimic in NSCLC cells and rescue the effects on NSCLC cells induced by miR-92a inhibitor; Taken together these findings suggested that miR-92a could promote growth metastasis and chemoresistance in NSCLC cells at least partially by targeting PTEN;MiR 92a Promotes Cell Metastasis of Colorectal Cancer Through PTEN Mediated PI3K/AKT Pathway; The expression of miR-92a PTEN and E-cadherin was analyzed by real-time PCR; In addition there was a negative correlation between levels of miR-92a and the PTEN gene p < 0.0001; The association of levels of miR-92a and PTEN with tumor cell migration in CRC was also confirmed in CRC cell models;MicroRNA miR-92 is overexpressed in a number of tumors and has been proven to negatively regulate a number of tumor suppressor genes including phosphatase and tensin homologue PTEN; PTEN protein expression was decreased in the SiHa cells that were transfected with the miR-92 mimic; The data indicated that miR-92 may increase the migration and invasion of SiHa cells partially through the downregulation of PTEN protein expression;Expression and significance of PTEN and miR 92 in hepatocellular carcinoma; Immunohistochemistry streptavidin-peroxidase SP and quantitative reverse transcriptase-polymerase chain reaction qRT‑PCR were used to detect the expression of PTEN and miR-92 in 15 cases of HCC and the corresponding paracancerous tissues; The correlation between PTEN and miR-92 was analyzed; Additionally the mRNA levels of PTEN and miR-92 showed a significantly negative correlation with each other r=-0.858 P<0.05; In conclusion PTEN and miR-92 have different roles in the development of HCC; The combined detection of PTEN and miR-92 may provide critical clinical evidence for the early diagnosis and prognosis of HCC;PTEN mRNA correlated inversely with miR-92a and members of the miR-17 and miR-130/301 families;The expression levels of miR-92a and phosphatase and tensin homologue PTEN were detected by qRT-PCR and western blot; In addition the regulation of PTEN by miR-92a was evaluated by qRT-PCR western blot and luciferase reporter assays; There was an inverse correlation between the levels of miR-92a and PTEN in CRC tissues; The overexpression of miR-92a in CRC cells decreased PTEN expression at the translational level and decreased PTEN-driven luciferase-reporter activity; Our results demonstrated that miR-92a induced EMT and regulated cell growth migration and invasion in the SW480 cells at least partially via suppression of PTEN expression	metastasis;drug resistance;metastasis;cell migration;;worse prognosis;;	lung squamous cell cancer;colorectal cancer;cervical and endocervical cancer;liver cancer;sarcoma;colorectal cancer
hsa-miR-93-5p	PTEN	1.50844106515467	1.83836866996875e-12	-0.41901734874011	0.000137135697667474	miRNAWalker2_validate;miRTarBase;miRNATAP	-0.209970443777429	3.2573256879644e-21	25633810;26243299;22465665;26087719	MicroRNA 93 activates c Met/PI3K/Akt pathway activity in hepatocellular carcinoma by directly inhibiting PTEN and CDKN1A; We confirmed that miR-93 directly bound with the 3' untranslated regions of the tumor-suppressor genes PTEN and CDKN1A respectivelyand inhibited their expression; We concluded that miR-93 stimulated cell proliferation migration and invasion through the oncogenic c-Met/PI3K/Akt pathway and also inhibited apoptosis by directly inhibiting PTEN and CDKN1A expression in human HCC;microRNA 93 promotes cell proliferation via targeting of PTEN in Osteosarcoma cells; An miRNA miR-93 was significantly up-regulated whereas phosphatase and tensin homologue PTEN expression was significantly down-regulated in all tested OS cells when compared with hMSCs; Ectopic expression of miR-93 decreased PTEN protein levels; Taking these observations together miR-93 can be seen to play a critical role in carcinogenesis through suppression of PTEN and may serve as a therapeutic target for the treatment of OS;Furthermore we found that miR-93 can directly target PTEN and participates in the regulation of the AKT signaling pathway; MiR-93 inversely correlates with PTEN expression in CDDP-resistant and sensitive human ovarian cancer tissues;Furthermore our study found berberine could inhibit miR-93 expression and function in ovarian cancer as shown by an increase of its target PTEN an important tumor suppressor in ovarian cancer; More importantly A2780 cells that were treated with PTEN siRNA had a survival pattern that is similar to cells with miR-93 overexpression	;tumorigenesis;;poor survival	liver cancer;sarcoma;ovarian cancer;ovarian cancer
hsa-let-7a-5p	RRM2	-1.37014061604018	3.11451492971224e-14	2.86899871288903	2.94977476028636e-19	miRNAWalker2_validate;TargetScan;miRNATAP	-0.577637163480958	1.21792374300508e-12		NA	NA	NA
hsa-let-7b-5p	RRM2	-1.62016148171663	1.56547487335694e-15	2.86899871288903	2.94977476028636e-19	miRNAWalker2_validate;miRNATAP	-0.642149930538833	9.54316290267664e-20		NA	NA	NA
hsa-let-7g-5p	RRM2	0.0837630831079359	0.583083118232597	2.86899871288903	2.94977476028636e-19	miRNAWalker2_validate;miRNATAP	-0.313003054815174	0.0021017280758929		NA	NA	NA
hsa-miR-142-3p	RRM2B	3.98476449801341	1.56256182021111e-35	-0.564869102427815	0.000329349327584025	miRNAWalker2_validate;miRanda	-0.120927069390427	4.99065993047701e-09		NA	NA	NA
hsa-miR-590-5p	RRM2B	2.07441240363458	4.95240551694843e-14	-0.564869102427815	0.000329349327584025	miRanda;mirMAP	-0.27932442631006	8.49259712160949e-20		NA	NA	NA
hsa-miR-30c-5p	SERPINE1	-0.327319105755825	0.123595832152687	-0.114178653022812	0.73682517077286	miRNAWalker2_validate;miRTarBase;MirTarget;miRNATAP	-0.284046002981584	0.00011264609085013		NA	NA	NA
hsa-miR-15a-5p	SESN1	1.62575353599172	1.55312121019827e-19	-1.80580674870285	1.4714514385367e-22	MirTarget;miRNATAP	-0.154734566762702	0.00122611667103779		NA	NA	NA
hsa-miR-28-5p	SESN1	1.19639196514745	4.59365801666536e-18	-1.80580674870285	1.4714514385367e-22	PITA;miRanda;miRNATAP	-0.207225809746842	0.00100137593234134		NA	NA	NA
hsa-miR-424-5p	SESN1	1.26485330287919	6.1498991028257e-06	-1.80580674870285	1.4714514385367e-22	MirTarget;miRNATAP	-0.121342221085396	0.000117496170259704		NA	NA	NA
hsa-miR-17-5p	SESN3	2.07078488653279	2.77403038572568e-19	-0.0968711060818062	0.738378790058081	MirTarget;TargetScan	-0.320514863614511	5.21782578112463e-09		NA	NA	NA
hsa-miR-25-3p	SESN3	0.361927330834176	0.0163670566170988	-0.0968711060818062	0.738378790058081	MirTarget;miRNATAP	-0.262570279749937	0.00329514714870453		NA	NA	NA
hsa-miR-29a-5p	SESN3	1.89519956688438	1.03453349363915e-11	-0.0968711060818062	0.738378790058081	MirTarget;mirMAP	-0.218202869457075	9.25535338942161e-05		NA	NA	NA
hsa-miR-32-5p	SESN3	0.876853679269853	6.04859399018691e-05	-0.0968711060818062	0.738378790058081	MirTarget;miRNATAP	-0.137797492746768	0.0372340815110363		NA	NA	NA
hsa-miR-320b	SESN3	0.226640952564488	0.378818692487242	-0.0968711060818062	0.738378790058081	miRanda;mirMAP	-0.166865438710542	0.00129195180283279		NA	NA	NA
hsa-miR-589-3p	SESN3	1.34253876396688	1.84935927493927e-05	-0.0968711060818062	0.738378790058081	MirTarget;mirMAP	-0.113732821954677	0.00909065981232026		NA	NA	NA
hsa-miR-590-3p	SESN3	0.83851360565783	0.00129224433453587	-0.0968711060818062	0.738378790058081	miRNAWalker2_validate;MirTarget;miRanda	-0.275497427158523	6.00422405103357e-06		NA	NA	NA
hsa-miR-7-1-3p	SESN3	2.61364240402652	1.98959237815786e-32	-0.0968711060818062	0.738378790058081	MirTarget;mirMAP	-0.19411315784066	0.00110224932445762		NA	NA	NA
hsa-miR-92a-3p	SESN3	-0.136362762339122	0.493412263619364	-0.0968711060818062	0.738378790058081	MirTarget;miRNATAP	-0.262781286032761	9.10655775232688e-05		NA	NA	NA
hsa-miR-96-5p	SESN3	3.0381097138467	4.40362891630201e-24	-0.0968711060818062	0.738378790058081	MirTarget;TargetScan	-0.18573570856152	0.000131001454194109		NA	NA	NA
hsa-miR-19a-3p	THBS1	2.11776595911517	7.07663078397156e-10	-0.930928104430071	0.00139531304277658	MirTarget;mirMAP	-0.320107454551527	1.0910865655915e-12		NA	NA	NA
hsa-miR-19b-3p	THBS1	2.10868505662119	5.40846613768389e-17	-0.930928104430071	0.00139531304277658	MirTarget;mirMAP	-0.394071669543936	1.30352702952378e-13		NA	NA	NA
hsa-miR-338-3p	THBS1	0.726843067232002	0.0506251324215494	-0.930928104430071	0.00139531304277658	MirTarget;PITA;miRanda	-0.137206796252208	0.000139893109055389		NA	NA	NA
hsa-miR-590-5p	THBS1	2.07441240363458	4.95240551694843e-14	-0.930928104430071	0.00139531304277658	miRanda;mirMAP	-0.246253114774633	2.83321183197093e-05		NA	NA	NA
hsa-miR-7-1-3p	THBS1	2.61364240402652	1.98959237815786e-32	-0.930928104430071	0.00139531304277658	MirTarget;mirMAP	-0.299067024820193	5.25045592977195e-07		NA	NA	NA
hsa-miR-429	ZMAT3	2.3794516574089	1.72813419703734e-13	-0.318761613695159	0.0781412592604581	MirTarget;miRNATAP	-0.104551391799815	0.000114833933352168		NA	NA	NA
hsa-miR-501-5p	ZMAT3	0.411357595674671	0.10435288464149	-0.318761613695159	0.0781412592604581	MirTarget;mirMAP	-0.223999145487047	3.62840278253431e-12		NA	NA	NA
hsa-miR-590-3p	ZMAT3	0.83851360565783	0.00129224433453587	-0.318761613695159	0.0781412592604581	mirMAP;miRNATAP	-0.143008576248367	0.000175656490032134		NA	NA	NA