miRNA	gene	miRNA_log2FC	miRNA_pvalue	gene_log2FC	gene_pvalue	interactions	correlation_beta	correlation_pvalue	PMID	evidence	outcome	cancer
hsa-miR-138-5p	ANGPT2	0.61608764992087	1.35200027885651e-05	-0.973073130335976	3.11405321255298e-13	MirTarget	-0.292625041668636	1.45807993019987e-12		NA	NA	NA
hsa-miR-138-5p	ANO6	0.61608764992087	1.35200027885651e-05	-0.362525289302433	8.04209213730108e-06	MirTarget	-0.222730538503581	1.67007991115467e-23		NA	NA	NA
hsa-miR-138-5p	ARHGAP42	0.61608764992087	1.35200027885651e-05	0.0716708840857936	0.38162071392574	MirTarget;miRNATAP	-0.155911910712092	1.47303233575759e-10		NA	NA	NA
hsa-miR-138-5p	ARRDC3	0.61608764992087	1.35200027885651e-05	-0.119441275627876	0.0481493321948708	miRNATAP	-0.136449410542342	2.6548341169657e-18		NA	NA	NA
hsa-let-7a-3p	ATRX	-0.0530563276543585	0.370749834463726	-0.000824434503044813	0.992488330570351	MirTarget;miRNATAP	-0.327151551755031	1.67188783570388e-06		NA	NA	NA
hsa-miR-106b-5p	ATRX	-0.167096183547595	0.0497544396383733	-0.000824434503044813	0.992488330570351	mirMAP	-0.17477001690392	0.000298655268852493		NA	NA	NA
hsa-miR-148b-5p	ATRX	-0.127111784487802	0.188731110216915	-0.000824434503044813	0.992488330570351	MirTarget	-0.115317210307527	0.00250837853022262		NA	NA	NA
hsa-miR-17-5p	ATRX	-0.097575136916686	0.206211102146113	-0.000824434503044813	0.992488330570351	miRNAWalker2_validate;mirMAP	-0.242766076015957	3.11304357626302e-05		NA	NA	NA
hsa-miR-186-5p	ATRX	-0.060638189413023	0.514217717592655	-0.000824434503044813	0.992488330570351	MirTarget;mirMAP	-0.433279156224759	6.25095647568981e-26		NA	NA	NA
hsa-miR-19a-3p	ATRX	-0.0466707843731764	0.576818938277875	-0.000824434503044813	0.992488330570351	MirTarget;miRNATAP	-0.191500579993004	2.46721609312968e-05		NA	NA	NA
hsa-miR-19b-3p	ATRX	0.013842745084812	0.856506310672867	-0.000824434503044813	0.992488330570351	MirTarget;miRNATAP	-0.2087267271675	0.000117314171102906		NA	NA	NA
hsa-miR-200c-3p	ATRX	-0.413752622631687	8.69363337156544e-06	-0.000824434503044813	0.992488330570351	MirTarget;miRNATAP	-0.186152278546305	1.51047726739901e-06		NA	NA	NA
hsa-miR-20a-5p	ATRX	0.0115865752289119	0.887069448775761	-0.000824434503044813	0.992488330570351	mirMAP	-0.121664028860004	0.0235258558376746		NA	NA	NA
hsa-miR-21-5p	ATRX	-1.05049251753105	2.58081295984588e-11	-0.000824434503044813	0.992488330570351	miRNAWalker2_validate	-0.105212144122095	4.65569044345593e-05		NA	NA	NA
hsa-miR-26b-5p	ATRX	0.0984536538763106	0.231803769574464	-0.000824434503044813	0.992488330570351	mirMAP	-0.255302292857077	1.19086316096028e-06		NA	NA	NA
hsa-miR-27a-3p	ATRX	-0.30376003289577	0.00457375391190104	-0.000824434503044813	0.992488330570351	miRNATAP	-0.103549587951637	0.00480440640701442		NA	NA	NA
hsa-miR-29a-5p	ATRX	0.0697727833812762	0.350621682973061	-0.000824434503044813	0.992488330570351	MirTarget	-0.118473607074149	0.0173373092413279		NA	NA	NA
hsa-miR-3065-5p	ATRX	0.262608140481518	0.0414570974147947	-0.000824434503044813	0.992488330570351	mirMAP	-0.345926927658	1.01191215667311e-39		NA	NA	NA
hsa-miR-30e-3p	ATRX	-0.00173769765871867	0.98496550154767	-0.000824434503044813	0.992488330570351	mirMAP	-0.267045607879499	6.18915669339815e-07		NA	NA	NA
hsa-miR-320c	ATRX	-0.343259124189967	0.000248338401291042	-0.000824434503044813	0.992488330570351	MirTarget;PITA;miRanda;miRNATAP	-0.118076077246345	0.00304879624175696		NA	NA	NA
hsa-miR-374b-3p	ATRX	-0.00769406264478012	0.897944859266225	-0.000824434503044813	0.992488330570351	MirTarget	-0.309577539025305	6.05945538175e-07		NA	NA	NA
hsa-miR-576-5p	ATRX	-0.106482276040039	0.194379152564202	-0.000824434503044813	0.992488330570351	mirMAP	-0.397467270714445	5.22502211299674e-20		NA	NA	NA
hsa-miR-590-3p	ATRX	-0.312951515438399	0.00048045542384394	-0.000824434503044813	0.992488330570351	MirTarget;PITA;miRanda;mirMAP;miRNATAP	-0.174926818850614	1.44994429685341e-05		NA	NA	NA
hsa-miR-590-5p	ATRX	-0.169460270359482	0.0386004382081766	-0.000824434503044813	0.992488330570351	miRanda	-0.147164492236566	0.00104043321246353		NA	NA	NA
hsa-miR-9-3p	ATRX	0.184945845984739	0.0290051908008628	-0.000824434503044813	0.992488330570351	MirTarget	-0.321358402869446	2.71839715593396e-08		NA	NA	NA
hsa-miR-92b-3p	ATRX	0.213968504162006	0.0523921855715249	-0.000824434503044813	0.992488330570351	MirTarget;miRNATAP	-0.251267823002937	2.82594742907409e-11		NA	NA	NA
hsa-miR-138-5p	BTG1	0.61608764992087	1.35200027885651e-05	-0.184952403664406	0.00164056003094408	miRNATAP	-0.125021304790807	8.59308691283892e-20		NA	NA	NA
hsa-miR-138-5p	CA3	0.61608764992087	1.35200027885651e-05	-1.27071401620038	5.5913267800272e-13	MirTarget	-0.26952646321806	1.2336280691904e-06		NA	NA	NA
hsa-miR-138-5p	CASP3	0.61608764992087	1.35200027885651e-05	-0.262751412479426	2.56855295665512e-06	miRNAWalker2_validate;miRTarBase	-0.113189968294872	3.60467356853659e-14		NA	NA	NA
hsa-miR-138-5p	CASP7	0.61608764992087	1.35200027885651e-05	-0.330891851472554	2.19049833744449e-07	MirTarget	-0.126194182155455	4.03886338228774e-11		NA	NA	NA
hsa-miR-138-5p	CD44	0.61608764992087	1.35200027885651e-05	-0.454265310281485	0.00121510157685102	MirTarget	-0.363787988084945	3.0607119194613e-19		NA	NA	NA
hsa-miR-138-5p	CD7	0.61608764992087	1.35200027885651e-05	-0.565636886892614	4.17985972756524e-06	mirMAP	-0.155395922543528	4.83498645280521e-05		NA	NA	NA
hsa-miR-138-5p	CEBPA	0.61608764992087	1.35200027885651e-05	-0.225572181260874	0.0334607671491343	miRNAWalker2_validate	-0.133070638427317	3.21414445973993e-05		NA	NA	NA
hsa-miR-138-5p	COL14A1	0.61608764992087	1.35200027885651e-05	-0.792131541926786	5.25794983899986e-07	MirTarget	-0.327759203128588	1.33004671541109e-11		NA	NA	NA
hsa-miR-138-5p	CSF3R	0.61608764992087	1.35200027885651e-05	-0.17270397871593	0.111444824636719	MirTarget	-0.139153549859984	2.30931003852574e-05		NA	NA	NA
hsa-miR-138-5p	CSRP2	0.61608764992087	1.35200027885651e-05	-0.25460400155885	0.0381419342799565	MirTarget	-0.256099209474651	3.5355836192218e-13		NA	NA	NA
hsa-miR-138-5p	CSTA	0.61608764992087	1.35200027885651e-05	-1.16683910109025	4.58965418347075e-09	MirTarget	-0.478688090745134	4.36997549781595e-15		NA	NA	NA
hsa-miR-138-5p	DDR1	0.61608764992087	1.35200027885651e-05	0.0224584798898135	0.770021963226609	mirMAP	-0.12767403701495	2.60998803600024e-15		NA	NA	NA
hsa-miR-138-5p	DDX11	0.61608764992087	1.35200027885651e-05	-0.310493120033059	0.000838793002332567	MirTarget	-0.143942876154978	2.80396692326931e-07		NA	NA	NA
hsa-miR-138-5p	DYNLT1	0.61608764992087	1.35200027885651e-05	-0.209857417082336	0.000632846447156105	MirTarget	-0.177014778917648	7.8191623600039e-28		NA	NA	NA
hsa-miR-105-5p	EGFR	0.567459149851699	8.20858944634191e-06	-0.375473556369595	0.0155485714375792	mirMAP	-0.353346118507539	9.24874721523108e-12		NA	NA	NA
hsa-miR-107	EGFR	0.121070851008406	0.19838128189417	-0.375473556369595	0.0155485714375792	miRanda	-0.160771846813735	0.0310898591296584		NA	NA	NA
hsa-miR-128-3p	EGFR	0.781932174412697	7.18127563212596e-10	-0.375473556369595	0.0155485714375792	miRNAWalker2_validate;miRTarBase	-0.123238476195056	0.0295408149966435		NA	NA	NA
hsa-miR-133a-3p	EGFR	0.335058908302962	0.018040278312104	-0.375473556369595	0.0155485714375792	miRNAWalker2_validate;miRTarBase;MirTarget	-0.240130883772277	1.69412746009746e-07	26138587;26076812;25903369;26134491;24816813;22407299;27465833;23786162	Growth of glioblastoma is inhibited by miR 133 mediated EGFR suppression; Bioinformatic analysis was performed showing that miR-133 may target the 3'-untranslated region 3'-UTR of the epidermal growth factor receptor EGFR that transduces cell growth signals; Further the protein translation inhibition of EGFR by miR-133 was confirmed by a dual luciferase reporter assay; Together these data suggest that reduced miR-133 levels in GBM tissues promotes cell growth and decreases cell apoptosis possibly through targeting mRNA of EGFR to suppress its translation;Moreover the 3'-untranslated region 3'UTR of Her-2 the epidermal growth factor receptor EGFR that transduces cell growth signals appeared to be targeted by miR-133;MiR-133a expression was negatively correlated to lymphatic metastasis r = -0.182 P = 0.042 tumor size r = -0.253 P = 0.04 clinical TNM stages r = -0.154 P = 0.087 and EGFR protein expression r = -0.612 P < 0.001;miR 133a inhibits cervical cancer growth by targeting EGFR; The epidermal growth factor receptor EGFR was confirmed to be a direct target of miR-133a in cervical cancer cells using luciferase assay and western blotting; Restoration of miR-133a inhibited EGFR expression and activated the AKT and ERK signaling pathways; These results showed that miR-133a suppresses cervical cancer growth in vitro and in vivo through targeting EGFR suggesting that miR-133a can be a potential target for the treatment of cervical cancer;MiR-133a can inhibit cell invasiveness and cell growth through suppressing the expressions of IGF-1R TGFBR1 and EGFR which then influences the downstream signaling in lung cancer cell lines;We also provide the first evidence that miR-133 may target EGFR;Epidermal growth factor receptor EGFR expression and Akt phosphorylation were significantly suppressed after miR-133a transfection by western blot detection; miR-133a suppressed cell proliferation by suppressing the expression of EGFR and the phosphorylation of Akt;Bioinformatics prediction showed that epidermal growth factor receptor EGFR is a potential target for miR-133a; A dual luciferase reporter gene assay showed that miR-133a bound to the 3' UTR of EGFR but not a mutated 3' UTR thereby down-regulating the protein expression level; Accordingly we found that expression of EGFR protein decreased with increased expression of miR-133a in MCF-7 and MDA-MB-231 cells; These results demonstrate that miR-133a which may act as a tumor suppressor in breast cancer regulates the cell cycle and proliferation in tumorigenesis by targeting EGFR through the downstream signal molecule Akt	;;staging;metastasis;tumor size;;;;;tumorigenesis	glioblastoma;gastric cancer;lung squamous cell cancer;cervical and endocervical cancer;lung squamous cell cancer;prostate cancer;breast cancer;breast cancer
hsa-miR-134-5p	EGFR	-0.0228681180463628	0.875465441075716	-0.375473556369595	0.0155485714375792	MirTarget	-0.131424347245258	0.0046901253546818	24440911;27241841	We show that the RTKs MET EGFR and PDGFR regulate microRNA-134 miR-134 in 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;Luciferase assays confirmed that EGFR is a direct target of miR-134; Further mechanistic investigation including RNAi and rescue experiments suggested that the down-regulation of EGFR by miR-134 partially contributes to the antiproliferative role of miR-134; Taken together our findings suggest that miR-134 inhibits non-small cell lung cancer growth by targeting the EGFR	;	glioblastoma;lung squamous cell cancer
hsa-miR-140-5p	EGFR	-0.0650635071034511	0.380452509211897	-0.375473556369595	0.0155485714375792	miRanda	-0.331443926880394	0.000604746363683769		NA	NA	NA
hsa-miR-141-3p	EGFR	-0.411205619919922	0.000393344390969032	-0.375473556369595	0.0155485714375792	MirTarget	-0.272211860280112	2.20526685695345e-06	26025929	Treatment with the EGFR inhibitor AG1478 or overexpression of miR141 blocked the activity of ERK downstream of EGFR and inhibited KLF8-depndent cell invasiveness proliferation and viability in cell culture and invasive growth and lung metastasis in nude mice	metastasis	breast cancer
hsa-miR-145-5p	EGFR	-0.108948399942988	0.310032352776812	-0.375473556369595	0.0155485714375792	miRTarBase	-0.222408723457338	0.000632008424910129	21653642;21289483;19493678	EGFR signals downregulate tumor suppressors miR 143 and miR 145 in Western diet promoted murine colon cancer: role of G1 regulators; Effects of EGFR on miR-143 and miR-145 expression were assessed in murine and human colonic cells and their putative targets examined in vitro and in vivo; EGFR signals suppressed miR-143 and miR-145 in human and murine colonic cells; EGFR suppresses miR-143 and miR-145 in murine models of colon cancer;MiR 145 inhibits cell proliferation of human lung adenocarcinoma by targeting EGFR and NUDT1; We previously reported that restoration of hsa-miR-145 inhibits cancer cell growth in lung adenocarcinoma patients with epidermal growth factor receptor EGFR mutation; The mRNA expressions of EGFR and NUDT1 were significantly downregulated after miR-145 transfection in human lung adenocarcinoma cells; Our results demonstrated miR-145 in the negative regulation of EGFR and NUDT1 expressions at both mRNA and protein levels; Upregulation of miR-145 appeared to be an important gene regulation mechanism for the proliferation of lung adenocarcinoma cells and it correlated strongly with the downregulation of EGFR and NUDT1; Our findings provided new insight into the complex regulating pathway comprising of miR-145 EGFR NUDT1 and other unknown factors which function in cell proliferation but not in apoptosis;Our results also show that restoration of tumour suppressor hsa-miR-145 inhibits cancer cell growth in EGFR mutant lung adenocarcinoma	;;	colon cancer;lung cancer;lung cancer
hsa-miR-146b-5p	EGFR	-0.441078059667276	0.000237619929889549	-0.375473556369595	0.0155485714375792	miRNATAP	-0.182905457755479	0.00149160880673993		NA	NA	NA
hsa-miR-148b-5p	EGFR	-0.127111784487802	0.188731110216915	-0.375473556369595	0.0155485714375792	mirMAP	-0.239934018287681	0.000528231733121031		NA	NA	NA
hsa-miR-17-5p	EGFR	-0.097575136916686	0.206211102146113	-0.375473556369595	0.0155485714375792	TargetScan	-0.300424779505137	0.00473688540815432		NA	NA	NA
hsa-miR-186-5p	EGFR	-0.060638189413023	0.514217717592655	-0.375473556369595	0.0155485714375792	mirMAP	-0.362820595408749	3.23429208060765e-06		NA	NA	NA
hsa-miR-199a-3p	EGFR	-0.412263318710744	0.000497136154474781	-0.375473556369595	0.0155485714375792	mirMAP	-0.155171655893965	0.00605438554579962		NA	NA	NA
hsa-miR-199b-3p	EGFR	-0.411848361704378	0.000517815011892612	-0.375473556369595	0.0155485714375792	mirMAP	-0.153587230840804	0.00647308065495246		NA	NA	NA
hsa-miR-21-5p	EGFR	-1.05049251753105	2.58081295984588e-11	-0.375473556369595	0.0155485714375792	miRNAWalker2_validate;miRTarBase	-0.118832377375515	0.0117576517085032	20113523;24012640;20048743;24198203;24331411;26563758;19597153;26026961	Thus the miR-21 inhibitor might interrupt the activity of EGFR pathways independently of PTEN status;Further the expression of miR-21 is regulated by EGFR via the activation of β-catenin and AP-1; These data indicate that a feedback loop exists between miR-21 and EGFR; These results clarify a novel association between miR-21 and EGFR in the regulation of cancer cell progression;Downregulation of miR 21 inhibits EGFR pathway and suppresses the growth of human glioblastoma cells independent of PTEN status;In radically resected NSCLC patients the expression levels of miR-21 10b in patients with EGFR mutation were much higher than those without mutation;MiR 21 overexpression is associated with acquired resistance of EGFR TKI in non small cell lung cancer;Higher expression levels of miR-21 AmiR-27a and miR-218 detected in this study suggest potential roles of these miRNAs in primary resistance to EGFR-TKI in advanced NSCLC patients with EGFR exon 19 deletion mutations;MiR 21 is an EGFR regulated anti apoptotic factor in lung cancer in never smokers; The changes in expression of some of these miRNAs including miR-21 were more remarkable in cases with EGFR mutations than in those without these mutations; In the never-smoker-derived lung adenocarcinoma cell line H3255 with mutant EGFR and high levels of p-EGFR and miR-21 antisense inhibition of miR-21 enhanced AG1478-induced apoptosis; In a never-smoker-derived adenocarcinoma cell line H441 with wild-type EGFR the antisense miR-21 not only showed the additive effect with AG1478 but also induced apoptosis by itself; These results suggest that aberrantly increased expression of miR-21 which is enhanced further by the activated EGFR signaling pathway plays a significant role in lung carcinogenesis in never-smokers as well as in smokers and is a potential therapeutic target in both EGFR-mutant and wild-type cases;Nickel may contribute to EGFR mutation and synergistically promotes tumor invasion in EGFR mutated lung cancer via nickel induced microRNA 21 expression	;progression;;;drug resistance;staging;drug resistance;tumorigenesis;	glioblastoma;glioblastoma;glioblastoma;lung squamous cell cancer;lung squamous cell cancer;lung squamous cell cancer;lung cancer;lung cancer
hsa-miR-27b-3p	EGFR	0.0599187745243448	0.582081434759731	-0.375473556369595	0.0155485714375792	MirTarget;miRNATAP	-0.221076471767459	0.000976089469884623		NA	NA	NA
hsa-miR-29a-5p	EGFR	0.0697727833812762	0.350621682973061	-0.375473556369595	0.0155485714375792	mirMAP	-0.214533796026545	0.0177106990395467	27477273	Feedback Loop Regulation of SCAP/SREBP 1 by miR 29 Modulates EGFR Signaling Driven Glioblastoma Growth		glioblastoma
hsa-miR-29b-2-5p	EGFR	0.268342619557287	0.00453760540519983	-0.375473556369595	0.0155485714375792	mirMAP	-0.358417872879751	3.99667666062669e-07		NA	NA	NA
hsa-miR-340-5p	EGFR	0.110504550202752	0.205224261934695	-0.375473556369595	0.0155485714375792	mirMAP	-0.346218765115495	1.66785221313902e-05		NA	NA	NA
hsa-miR-342-3p	EGFR	0.125683829770898	0.105810751640081	-0.375473556369595	0.0155485714375792	miRanda	-0.663917527907302	1.30767225931049e-12		NA	NA	NA
hsa-miR-362-5p	EGFR	0.0730185557229386	0.425572997292157	-0.375473556369595	0.0155485714375792	mirMAP	-0.425583661873956	4.49473787679401e-09		NA	NA	NA
hsa-miR-3622a-3p	EGFR	-0.0389203848593475	0.756058129624588	-0.375473556369595	0.0155485714375792	mirMAP	-0.122889761271843	0.0226283276731711		NA	NA	NA
hsa-miR-374a-3p	EGFR	-0.176226170437582	0.0343958848425882	-0.375473556369595	0.0155485714375792	mirMAP	-0.362986532828884	0.000239618326261467		NA	NA	NA
hsa-miR-374b-3p	EGFR	-0.00769406264478012	0.897944859266225	-0.375473556369595	0.0155485714375792	mirMAP	-0.427233704833407	0.000162731500775749		NA	NA	NA
hsa-miR-375	EGFR	0.0268401141324208	0.858358101444604	-0.375473556369595	0.0155485714375792	miRanda	-0.169128003930842	0.000103586363427282		NA	NA	NA
hsa-miR-432-5p	EGFR	0.214242438141989	0.166186087759922	-0.375473556369595	0.0155485714375792	mirMAP	-0.131937974290007	0.0019216701815729		NA	NA	NA
hsa-miR-455-5p	EGFR	-0.332224239762001	0.0106491358056235	-0.375473556369595	0.0155485714375792	miRanda	-0.204812179021233	5.18972286460639e-05		NA	NA	NA
hsa-miR-490-3p	EGFR	0.834268051506887	5.26203010743174e-06	-0.375473556369595	0.0155485714375792	miRNATAP	-0.120072101708822	0.00092511979931243		NA	NA	NA
hsa-miR-491-5p	EGFR	0.749881113074991	8.22859263178918e-09	-0.375473556369595	0.0155485714375792	miRanda	-0.15355901980036	0.00200795950337826	25299770	This latter effect is due to direct targeting of epidermal growth factor receptor EGFR by miR-491-5p and consequent inhibition of downstream AKT and MAPK signalling pathways; Induction of apoptosis by miR-491-5p in this cell line is mimicked by a combination of EGFR inhibition together with a BH3-mimetic molecule		ovarian cancer
hsa-miR-501-5p	EGFR	-0.0878951859817464	0.309663377222435	-0.375473556369595	0.0155485714375792	mirMAP	-0.204458704242994	0.00778191664099004		NA	NA	NA
hsa-miR-539-5p	EGFR	0.326485413953599	0.0554453076411236	-0.375473556369595	0.0155485714375792	MirTarget;mirMAP	-0.164306654210725	1.88169889749939e-05		NA	NA	NA
hsa-miR-542-3p	EGFR	-0.0835995677900652	0.403838744494172	-0.375473556369595	0.0155485714375792	miRanda	-0.200337541146819	0.00617654519167961		NA	NA	NA
hsa-miR-577	EGFR	0.382068371859265	0.0145513192729146	-0.375473556369595	0.0155485714375792	mirMAP	-0.117018511597701	0.00601694200161573		NA	NA	NA
hsa-miR-590-3p	EGFR	-0.312951515438399	0.00048045542384394	-0.375473556369595	0.0155485714375792	mirMAP	-0.214045002105238	0.00365962356824128		NA	NA	NA
hsa-miR-654-3p	EGFR	0.00355488592828523	0.979671440962753	-0.375473556369595	0.0155485714375792	mirMAP	-0.128189186321505	0.00719754733314809		NA	NA	NA
hsa-miR-7-1-3p	EGFR	0.0894475316162513	0.373223597851017	-0.375473556369595	0.0155485714375792	mirMAP	-0.276379724120531	2.83072126766495e-05		NA	NA	NA
hsa-miR-767-3p	EGFR	0.429854368420513	0.000821445291167693	-0.375473556369595	0.0155485714375792	MirTarget;PITA	-0.130739566149441	0.0130000034790611		NA	NA	NA
hsa-miR-769-5p	EGFR	0.320572895263089	0.00425481410304189	-0.375473556369595	0.0155485714375792	mirMAP	-0.16419521509748	0.00642768950459396		NA	NA	NA
hsa-miR-877-5p	EGFR	0.0775421790642759	0.423413623033694	-0.375473556369595	0.0155485714375792	mirMAP	-0.212946423195282	0.00180004411848772		NA	NA	NA
hsa-miR-138-5p	EIF4EBP1	0.61608764992087	1.35200027885651e-05	-0.345125060464951	2.64227717559213e-05	MirTarget;miRNATAP	-0.193406903930313	4.6473196917631e-16		NA	NA	NA
hsa-miR-138-5p	ENG	0.61608764992087	1.35200027885651e-05	-0.512138061598542	1.40697007867412e-11	miRNATAP	-0.126835473141255	5.17219068996492e-09		NA	NA	NA
hsa-miR-138-5p	ERI1	0.61608764992087	1.35200027885651e-05	-0.278415260868348	4.73505527570914e-08	MirTarget	-0.138616179634239	6.96424142059147e-23		NA	NA	NA
hsa-miR-138-5p	EZH2	0.61608764992087	1.35200027885651e-05	-0.760319021185372	9.56079034520981e-13	miRNAWalker2_validate;MirTarget;miRNATAP	-0.237697173917202	2.84752840689504e-13	23343715;27019355;25994569;24406044;27562865	MiR 138 inhibits tumor growth through repression of EZH2 in non small cell lung cancer; Furthermore knockdown of EZH2 phenocopied the tumor suppressive effects of miR-138 in cell models whereas ectopic expression of EZH2 rescued the suppressive effects of miR-138;MiR 138 Acts as a Tumor Suppressor by Targeting EZH2 and Enhances Cisplatin Induced Apoptosis in Osteosarcoma Cells; We also verified that EZH2 is a direct target of miR-138; Furthermore enhancing EZH2 expression reduced the inhibitory effects of miR-138 on osteosarcoma;FOXP4 downregulation-mediated inhibition on cancer cell growth and invasion was independent on overexpressing EZH2 another direct target of miR-138 in NSCLC;MiR 138 induces renal carcinoma cell senescence by targeting EZH2 and is downregulated in human clear cell renal cell carcinoma; Transfection of miR-138 mimic induced SN-12 cell senescence decreased the protein expression of EZH2 and increased the protein expression of P16; Furthermore miR-138 decreased the 3'UTR luciferase activity of EZH2; MiR-138 is a tumor-suppressor miRNA in ccRCC that induces SN-12 cell senescence by downregulating EZH2 expression and upregulating P16 expression;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	;;;;	lung squamous cell cancer;sarcoma;lung squamous cell cancer;kidney renal cell cancer;prostate cancer
hsa-miR-138-5p	FABP4	0.61608764992087	1.35200027885651e-05	-0.267269846450669	0.106061542427622	miRNAWalker2_validate	-0.220884030580769	1.54353932929917e-05		NA	NA	NA
hsa-miR-138-5p	FERMT2	0.61608764992087	1.35200027885651e-05	-0.00120937969482426	0.984045000610651	MirTarget;miRNATAP	-0.103729148712908	3.89151158074309e-13		NA	NA	NA
hsa-miR-138-5p	FOSL1	0.61608764992087	1.35200027885651e-05	-1.03487462222003	4.87762882989885e-12	miRTarBase	-0.284692328939477	1.19315764301941e-09		NA	NA	NA
hsa-miR-138-5p	GALNT10	0.61608764992087	1.35200027885651e-05	-0.13446752263483	0.08490334459581	MirTarget	-0.11804398114353	5.01080796911833e-08		NA	NA	NA
hsa-miR-138-5p	H3F3B	0.61608764992087	1.35200027885651e-05	0.0117731638707692	0.862274016237514	MirTarget;miRNATAP	-0.112519736665135	1.2361351438559e-19		NA	NA	NA
hsa-miR-138-5p	H6PD	0.61608764992087	1.35200027885651e-05	-0.202434637783599	0.00105942009343447	mirMAP	-0.122030444467088	1.11257564146978e-14		NA	NA	NA
hsa-miR-138-5p	HIF1A	0.61608764992087	1.35200027885651e-05	0.00484625688145268	0.948287190529189	miRNAWalker2_validate;miRTarBase	-0.165502020945438	2.83284283527236e-20	21875287	Western blot and reporter assays were used to assess HIF-1a as a direct target of miR-138; The data showed HIF-1a to be one target of miR-138; Futhermore inhibition of the expression of HIF-1a with specific siRNA or miR-138 could increase apoptosis and reduce the migration of 786-O cells; miR-138 could inhibit the expression of HIF-1a and regulate the apoptosis and migration of ccRCC cells		kidney renal cell cancer
hsa-miR-129-5p	IDH1	0.567133990117154	0.00116152215679873	-0.216141444909924	0.000633777977382499	miRanda	-0.125494153455114	2.54137708167644e-22		NA	NA	NA
hsa-miR-23b-3p	IDH1	-0.0476610245859863	0.630277683372509	-0.216141444909924	0.000633777977382499	MirTarget;miRNATAP	-0.158144158407436	7.58509880202707e-10		NA	NA	NA
hsa-miR-30a-5p	IDH1	0.0629429366112948	0.513851954699872	-0.216141444909924	0.000633777977382499	miRNAWalker2_validate;miRNATAP	-0.299743196511928	7.36626690045671e-15		NA	NA	NA
hsa-miR-30c-5p	IDH1	0.0469114469943488	0.565934557464302	-0.216141444909924	0.000633777977382499	miRNATAP	-0.24748288960472	4.12739260346008e-12		NA	NA	NA
hsa-miR-30d-5p	IDH1	0.0607010868720561	0.471410043548418	-0.216141444909924	0.000633777977382499	miRNATAP	-0.282569749093469	3.8309339817106e-12		NA	NA	NA
hsa-miR-338-3p	IDH1	0.399637046793888	0.00344106432206527	-0.216141444909924	0.000633777977382499	miRanda	-0.123191660416882	1.15883998831443e-11		NA	NA	NA
hsa-miR-362-5p	IDH1	0.0730185557229386	0.425572997292157	-0.216141444909924	0.000633777977382499	MirTarget	-0.143082256094293	1.57991965009734e-08		NA	NA	NA
hsa-miR-421	IDH1	0.171573235029884	0.0518112933650958	-0.216141444909924	0.000633777977382499	PITA;miRanda	-0.104039701706185	6.79097227937318e-05		NA	NA	NA
hsa-miR-543	IDH1	0.347737549779626	0.0157394585079679	-0.216141444909924	0.000633777977382499	miRanda	-0.10435629547451	8.20046830014469e-11		NA	NA	NA
hsa-miR-7-1-3p	IDH1	0.0894475316162513	0.373223597851017	-0.216141444909924	0.000633777977382499	MirTarget	-0.19192531211932	1.06583767981504e-17		NA	NA	NA
hsa-miR-138-5p	INHBB	0.61608764992087	1.35200027885651e-05	-0.0251327625400433	0.774840472524573	miRNATAP	-0.128623508013105	1.16707558738966e-06		NA	NA	NA
hsa-miR-138-5p	LSM14A	0.61608764992087	1.35200027885651e-05	-0.135675532863164	0.0197385310025792	MirTarget;miRNATAP	-0.109650058163427	2.56777522172665e-17		NA	NA	NA
hsa-miR-138-5p	MOV10	0.61608764992087	1.35200027885651e-05	-0.310633126595345	5.47469034952456e-06	MirTarget;miRNATAP	-0.176499754078797	2.17594094768508e-20		NA	NA	NA
hsa-miR-138-5p	MYD88	0.61608764992087	1.35200027885651e-05	-0.413794389705457	3.45628586506132e-06	MirTarget	-0.14950820343919	1.68371091611091e-08		NA	NA	NA
hsa-miR-138-5p	NFIB	0.61608764992087	1.35200027885651e-05	0.151336169908435	0.0298860513853786	miRNATAP	-0.119145068140554	1.42900410001137e-11		NA	NA	NA
hsa-miR-138-5p	OAS3	0.61608764992087	1.35200027885651e-05	-0.476505986488794	1.01093429474311e-05	miRNATAP	-0.131436719629714	7.47018588804762e-05		NA	NA	NA
hsa-miR-138-5p	PDE3A	0.61608764992087	1.35200027885651e-05	0.241260329299709	0.0680836729875631	miRNATAP	-0.135289379379272	0.000916778378804468		NA	NA	NA
hsa-miR-138-5p	PDPN	0.61608764992087	1.35200027885651e-05	-1.00574945169594	1.60350453569877e-07	MirTarget	-0.251280056416012	2.8072610678822e-05		NA	NA	NA
hsa-miR-138-5p	PLD2	0.61608764992087	1.35200027885651e-05	-0.012178025243057	0.838496276273452	MirTarget	-0.11260331070407	6.83689923086335e-13		NA	NA	NA
hsa-miR-138-5p	PLEK2	0.61608764992087	1.35200027885651e-05	-1.14950731519334	1.25610000852046e-13	miRNAWalker2_validate	-0.212403842778221	1.39797005593219e-05		NA	NA	NA
hsa-miR-138-5p	PLXNB2	0.61608764992087	1.35200027885651e-05	-0.132647321414402	0.0224282194893427	MirTarget;miRNATAP	-0.124434716986312	6.24688996245766e-23		NA	NA	NA
hsa-miR-138-5p	POFUT2	0.61608764992087	1.35200027885651e-05	-0.0888309271662386	0.0704201719803718	mirMAP	-0.105877080963887	3.99574176823053e-18		NA	NA	NA
hsa-miR-138-5p	RAVER1	0.61608764992087	1.35200027885651e-05	-0.20765642300109	0.000210008273604412	MirTarget	-0.14326880920348	1.80492527389965e-28		NA	NA	NA
hsa-miR-138-5p	RELA	0.61608764992087	1.35200027885651e-05	-0.0739196932169728	0.126314845681894	miRNATAP	-0.118615517312994	4.30114332551203e-37		NA	NA	NA
hsa-miR-138-5p	RHOC	0.61608764992087	1.35200027885651e-05	-0.360474333884857	1.02894564375166e-05	miRNAWalker2_validate;miRTarBase;MirTarget;miRNATAP	-0.160452198953384	1.02289321769822e-13	24565984	We hypothesize that miR-138 can inhibit the function of RhoC and consequently the activation of downstream target molecules involve in the signaling cascade; Data obtained by G-LISA and real time PCR shows an inverse correlation between RhoC expression and miR-138 in HNSCC cell lines; Additionally we obtained a similar pattern of RhoC and miR-138 expression in primary tumors from HNSCC patients; Over expression of miR-138 in HNSCC lines showed down regulation of RhoC as well as a decrease in cell motility invasion colony and stress fiber formation; These findings strongly suggest that the inhibition of RhoC can be achieved by over expressing miR-138 which further attenuates the downstream signaling cascade leading to cancer progression and survival	motility;progression;poor survival	head and neck cancer
hsa-miR-138-5p	RP2	0.61608764992087	1.35200027885651e-05	-0.151504636084979	0.0113013203152822	MirTarget	-0.153954682248414	4.6557110741161e-21		NA	NA	NA
hsa-miR-138-5p	RPS6KA1	0.61608764992087	1.35200027885651e-05	-0.28845668158696	0.00241163224126914	MirTarget;miRNATAP	-0.100557924867178	0.000472980824832504		NA	NA	NA
hsa-miR-138-5p	S100A2	0.61608764992087	1.35200027885651e-05	-0.394696364077724	0.00184425931521286	MirTarget	-0.26037997610956	1.8185086775926e-11		NA	NA	NA
hsa-miR-138-5p	SERPINE1	0.61608764992087	1.35200027885651e-05	-1.27620546981703	1.9162673271459e-12	miRNAWalker2_validate	-0.27183048471367	1.58790910020002e-06		NA	NA	NA
hsa-miR-138-5p	SH3BP2	0.61608764992087	1.35200027885651e-05	-0.0151935322989249	0.835246771220392	mirMAP	-0.139619832259279	2.62542234625888e-12		NA	NA	NA
hsa-miR-138-5p	SH3PXD2B	0.61608764992087	1.35200027885651e-05	-0.232442110520861	0.000432599553935746	mirMAP	-0.120760461146284	1.34458659783046e-12		NA	NA	NA
hsa-miR-138-5p	SIX5	0.61608764992087	1.35200027885651e-05	-0.184844151712891	0.0438990118844804	MirTarget	-0.182676715965195	2.88245139891821e-11		NA	NA	NA
hsa-miR-138-5p	SKP2	0.61608764992087	1.35200027885651e-05	-0.304483103342994	2.39516717741556e-06	MirTarget	-0.112767222560839	6.70974775053186e-09		NA	NA	NA
hsa-miR-138-5p	SNX20	0.61608764992087	1.35200027885651e-05	-0.0188096130981563	0.853361162479147	MirTarget	-0.16902471814797	5.84763689412306e-08		NA	NA	NA
hsa-miR-138-5p	SOX11	0.61608764992087	1.35200027885651e-05	-0.269962225683294	0.0274165085032646	mirMAP	-0.142534792030855	9.59090455827983e-05		NA	NA	NA
hsa-miR-138-5p	SOX4	0.61608764992087	1.35200027885651e-05	-0.130399677516149	0.285587017757533	miRNAWalker2_validate;MirTarget;miRNATAP	-0.176228798042081	3.86797942730557e-07	23389731	Results indicated that miR-138 directly targeted SRY-related high mobility group box 4 SOX4 and hypoxia-inducible factor-1α HIF-1α and overexpression of SOX4 and HIF-1α effectively reversed the miR-138-mediated suppression of cell invasion; Analysis of human ovarian tumors further revealed downregulation of miR-138 and upregulation of SOX4 in late-stage tumors; Our study demonstrates the role and clinical relevance of miR-138 in ovarian cancer cell invasion and metastasis providing a potential therapeutic strategy for suppression of ovarian cancer metastasis by targeting SOX4 and HIF-1α pathways	staging;metastasis	ovarian cancer
hsa-miR-138-5p	SPN	0.61608764992087	1.35200027885651e-05	-0.391372008456832	0.000280443010993604	mirMAP	-0.200940450248522	1.37796682612817e-09		NA	NA	NA
hsa-miR-138-5p	SRGAP1	0.61608764992087	1.35200027885651e-05	-0.20363001724538	0.00127045832139932	mirMAP	-0.124954489829075	4.17044105914372e-14		NA	NA	NA
hsa-miR-138-5p	STK40	0.61608764992087	1.35200027885651e-05	-0.425259479771283	5.47212717835944e-10	mirMAP	-0.116364289774095	9.57489204048645e-10		NA	NA	NA
hsa-miR-138-5p	TEAD1	0.61608764992087	1.35200027885651e-05	0.00514554964397007	0.94008046165122	MirTarget	-0.115112209225569	1.50230673879044e-11		NA	NA	NA
hsa-miR-138-5p	TET2	0.61608764992087	1.35200027885651e-05	0.116190829615161	0.0502346539924286	miRNATAP	-0.100026980181547	1.4603090478491e-10		NA	NA	NA
hsa-miR-138-5p	TMEM154	0.61608764992087	1.35200027885651e-05	-0.671920326082807	1.02846112022968e-10	MirTarget	-0.188443007596674	6.48237206507863e-09		NA	NA	NA
hsa-miR-138-5p	TMEM37	0.61608764992087	1.35200027885651e-05	-0.431482715678638	4.33191357428604e-07	MirTarget	-0.168095098869245	1.7150515203529e-10		NA	NA	NA
hsa-miR-125a-5p	TP53	0.0833349424517795	0.32544020025337	-0.346312114104129	1.42081328137354e-05	miRNAWalker2_validate;miRTarBase;miRanda	-0.375445863722298	1.2184854773952e-16	26389681;21777146;23079745	Mechanistically inactivation of miR-125a during cervical carcinogenesis was caused by HPV suppression of p53 expression;In addition wild-type p53 mRNA and protein expression was increased by hsa-miR-125a-5p overexpression; Moreover blocking wild-type p53 attenuated the effect of hsa-miR-125a-5p on apoptosis; In loss-of-function experiments wild-type p53 mRNA and protein expression was decreased by blocking hsa-miR-125a-5p; The effect of hsa-miR-125a-5p inhibitor on apoptosis was also weakened by blocking wild-type p53;Furthermore treatment of HCC cells with 5-aza-2'-deoxycytidine or ectopic expression of wildtype but not mutated p53 restored miR-125a-5p and miR-125b expression and inhibited tumor cell growth suggesting their regulation by promoter methylation and p53 activity	tumorigenesis;;	cervical and endocervical cancer;lung cancer;liver cancer
hsa-miR-125b-5p	TP53	0.0119698382910922	0.890233923196969	-0.346312114104129	1.42081328137354e-05	miRNAWalker2_validate;miRTarBase	-0.294628443669371	1.07324994036762e-07	24169356;24846940;26335100;24137477;26686386;24402874;21399871;23585871;24762088;23079745	MiR 125b acts as an oncogene in glioblastoma cells and inhibits cell apoptosis through p53 and p38MAPK independent pathways; Further studies reveal that p53 is regulated by miR-125b; However downregulation of the endogenous miR-125b also results in p53-independent apoptotic pathway leading to apoptosis in p53 mutated U251 cells and p53 knockdown U87 cells;The results revealed that hsa-miR-125b may regulate multiple biological processes and signal transduction pathways and drug-resistant occurrence is associated with cell proliferation cell apoptosis cell cycle and signaling pathways including MAPK Wnt and p53;The carboxy terminal domain of connexin 43 CT Cx43 modulates the expression of p53 by altering miR 125b expression in low grade human breast cancers; In addition CT-Cx43 was exogenously expressed in the breast cancer-derived cell line MCF-7 and its effect on the expression of miR-125b and its downstream target p53 were evaluated as well as its effect on cellular proliferation and death using MTT and LDH assays respectively; Interestingly we found that miR-125b a negative regulator of p53 exhibited an inverse expression relationship with CT-Cx43 in the breast cancer samples tested;TP53 and hsa-miR-125b were observed to form a self-adaptation association;In this study we have investigated the delivery and transfection of wild-type wt- p53 and microRNA-125b miR-125b expressing plasmid DNA in SK-LU-1 human lung adenocarcinoma cells as well as in KrasG12D/p53fl/fl KP genetically engineered mouse model of lung cancer;miR-34a is directly regulated by p53 and acts as tumor suppressor while miR-125b plays a significant role in immune response and apoptosis;In vitro assays revealed that overexpression of miR-125b repressed the endogenous level of p53 protein in human colorectal cancer cells;In this study we further extend our studies by showing that miR-125b represses the protein product of the ink4a/ARF locus p14ARF in two prostate cancer cell lines LNCaP wild type-p53 and 22Rv1 both wild type and mutant p53 as well as in the PC-346C prostate cancer xenograft model that lentivirally overexpressed miR-125b;A stable overexpression of miR-125b in human melanoma cell line Mel-Juso resulted in a G0/G1 cell cycle block and emergence of large cells expressing senescence markers: senescence-associated beta-galactosidase p21 p27 and p53;Furthermore treatment of HCC cells with 5-aza-2'-deoxycytidine or ectopic expression of wildtype but not mutated p53 restored miR-125a-5p and miR-125b expression and inhibited tumor cell growth suggesting their regulation by promoter methylation and p53 activity; To show the clinical significance of these findings mutations in the DNA binding domain of p53 and promoter methylation of miR-125b were investigated; Four out of nine patients with induced SIRT7 carried mutations in the p53 gene and one patient showed hypermethylation of the miR-125b promoter region	;;;;;immune resistance;;;;	glioblastoma;gastric cancer;breast cancer;pancreatic cancer;lung cancer;cervical and endocervical cancer;colorectal cancer;prostate cancer;melanoma;liver cancer
hsa-miR-150-5p	TP53	-0.0645271721519425	0.51329565882884	-0.346312114104129	1.42081328137354e-05	miRNAWalker2_validate	-0.156281214913021	3.09404029899862e-06	23747308;23228962	miR 150 promotes the proliferation of lung cancer cells by targeting P53; Here we demonstrate that miR-150 is aberrantly upregulated in lung cancer tissue and negatively correlates with the expression of the proapoptotic gene p53 but not EGR2; We show that miR-150 specifically targets the 3'-UTR of p53 and regulates its expression; Inhibition of miR-150 effectively delays cell proliferation and promotes apoptosis accompanied by increased p53 protein expression;miR-150 and miR-3940-5p were found to be significantly downregulated in p53 IHC-positive NSCLC cases and were negatively correlated with p53 mRNA; miR-150 and miR-3940-5p may affect p53 expression through a direct or indirect pathway	;	lung cancer;lung squamous cell cancer
hsa-miR-221-3p	TP53	0.010950728507197	0.936440693394406	-0.346312114104129	1.42081328137354e-05	miRNAWalker2_validate	-0.143405645468124	6.89189438710031e-10	20880178;24324033	Circulating miR 221 directly amplified from plasma is a potential diagnostic and prognostic marker of colorectal cancer and is correlated with p53 expression; The correlation between miR-221 levels and protein levels of p53 CEA ER and PR clinicopathological features or overall survival was analyzed; The immunohistochemistry analysis demonstrates a significant correlation between plasma miR-221 level and p53 expression; The direct amplification of plasma miR-221 can be used as a potential noninvasive molecular marker for diagnosis and prognosis of CRC and is correlated with p53 expression;Interestingly miR-221 can activate the p53/mdm2 axis by inhibiting MDM2 and in turn p53 activation contributes to miR-221 enhanced expression; Moreover by modulating the p53 axis miR-221 impacts cell-cycle progression and apoptotic response to doxorubicin in hepatocellular carcinoma-derived cell lines; These data were confirmed in clinical specimens of hepatocellular carcinoma in which elevated miR-221 expression was associated with the simultaneous presence of wild-type p53 and DNA hypomethylation	poor survival;worse prognosis;progression;drug resistance	colorectal cancer;liver cancer
hsa-miR-222-3p	TP53	-0.107117065575191	0.423818119725726	-0.346312114104129	1.42081328137354e-05	miRNAWalker2_validate	-0.142653482163308	1.2671214916531e-09		NA	NA	NA
hsa-miR-30d-5p	TP53	0.0607010868720561	0.471410043548418	-0.346312114104129	1.42081328137354e-05	miRNAWalker2_validate	-0.336903694979927	3.32137008004591e-09		NA	NA	NA
hsa-miR-324-5p	TP53	-0.0183370482495828	0.842996782677376	-0.346312114104129	1.42081328137354e-05	miRNAWalker2_validate	-0.170645382602635	1.21583558752455e-06		NA	NA	NA
hsa-miR-338-3p	TP53	0.399637046793888	0.00344106432206527	-0.346312114104129	1.42081328137354e-05	miRanda	-0.117560999445537	4.2049029410775e-06		NA	NA	NA
hsa-miR-34a-5p	TP53	-0.143472919835505	0.211283228567119	-0.346312114104129	1.42081328137354e-05	miRNAWalker2_validate	-0.127236433475415	7.74576992902642e-06	23155233;19773441;25572695;25123132;22438124;21702042;22292433;21383543;25982144;19443717;26790955;24642471;22198213;25362853;23036084;19421141;24444609;20186752;22457788;27186405;21731696;19736307;26879132;23569431;25771001;23292869;24209638;24957404;21240262;24503183;22102859;18803879;24630988;25895459;25894979;19714243;26944831;19921694;21909380;25789847;23450486;24402874;24337371;18497571;25490093;22593438;24528540;20145172;23349340;25038915;21321636;23632240;23624843;19029026;20309940;22810507;23862748;25932212;18834855;21225432	The high miR-34a expression level in the cells after irradiation at 60 Gy reduced the p53 expression level;MicroRNA-34a miR-34a is a transcriptional target of p53 that is down-regulated in some cancer cell lines; Analysis of human specimens showed that miR-34a expression is down-regulated in glioblastoma tissues as compared with normal brain and in mutant p53 gliomas as compared with wild-type p53 gliomas;For this purpose cell viability assay Realtime quantitative PCR for mRNA quantification western blot for essential protein expression p53 silencing by shRNA and miR-34a knockdown were performed in the present study; PRE also elevated p53 protein and triggered miR-34a expression;As expected p53 loss caused downregulation of established p53 targets e.g p21 and miR-34 family and increased proliferation in both luminal and basal-like cell lines;Moreover re-expression of miR-34a by transfection in NSCLC cells resulted in inhibition of cell growth and invasiveness induction of apoptosis and enhanced p53 activity;MiR 34a chemosensitizes bladder cancer cells to cisplatin treatment regardless of p53 Rb pathway status; MiR-34a is a downstream effector of p53 that has been shown to target several molecules associated with cell cycle and cell survival pathways; As alterations in these pathways are frequent in muscle invasive transitional cell carcinoma of the bladder MI-TCC for example mutation or loss of p53 and Rb the goal of this study was to determine whether manipulation of miR-34a expression levels could abrogate the effect of these alterations and sensitize bladder cancer cells to chemotherapy;Reporter assay further showed that NF-kappaB-induced miR-34a transcriptional activity was reduced by p53 impairment; And wildtype p53 is responsible for NF-kappaB-mediated miR-34a transcriptional activity but not for NF-kappaB binding;Recently miR-34 family has been shown to be part of the p53 pathway which is frequently involved in lung cancer and the expression of miR-34 has been reported to be regulated by DNA methylation;5 Aminolevulinic acid mediated sonodynamic therapy induces anti tumor effects in malignant melanoma via p53 miR 34a Sirt1 axis; Therefore the p53 miR-34a and SIRT1 constituted a positive feedback loop;miR-34a expression could be increased in Y79 cells but not Weri-Rb1 cells after p53 activation; This differential regulation was not caused by genomic alterations at the miR-34a p53 binding site or mature gene;Conversely kallistatin stimulated expression of the tumorigenic suppressors miR-34a and p53;Members of the miR-34 family are induced by the tumor suppressor p53 and are known to inhibit epithelial-to-mesenchymal transition EMT and therefore presumably suppress the early phases of metastasis;MicroRNA-34a miR-34a a transcriptional target of p53 is a well-known tumor suppressor gene; Moreover we found that miR-34a was downregulated in 25 of 40 62.5% colon cancer tissues as compared with the adjacent normal colon tissues and that the expression of miR-34a was correlated with the DNA-binding activity of p53;Ectopic expression of miR-34a-5p in p53 wild-type colon cancer cell HCT116 significantly inhibited cell growth migration invasion and metastasis; miR-34a-5p induced cell apoptosis cell cycle arrest at G1 phase and p53 transcription activity in HCT116 cells but not in the HCT116 p53 knockout p53-/- cells; miR-34a-5p significantly suppressed the HCT116 growth in vivo whereas it showed no effect on the HCT116 p53-/- xenograft indicating that the growth-inhibiting effect by miR-34a-5p was dependent on p53;microRNA 34a sensitizes lung cancer cell lines to DDP treatment independent of p53 status; However the precise biological role of miR-34a in p53 deficient lung cancer cell lines remains largely elusive; Overall in this study we found the proliferation inhibition function of miR-34a in vitro in lung cancer cell lines is p53 independent and also demonstrated the combination therapeutic potential of miR-34a and DDP in lung cancer cell lines;In particular mammalian miR-34 is upregulated by p53 in response to radiation but little is known about the role of this miRNA in vivo; These findings show a role for mir-34 in both apoptotic and non-apoptotic cell death in vivo much like that of cep-1 the C elegans p53 homolog;Tumor-suppressive miR-34a a direct target of p53 has been shown to target several molecules of cell survival pathways; Here we show that capsaicin-induced oxidative DNA damage culminates in p53 activation to up-regulate expression of miR-34a in non-small cell lung carcinoma NSCLC cells;Accumulating evidence suggests that miR-34a as a key mediator of p53 tumor suppression is aberrantly expressed in human cancers; Bioinformatics analysis produced a protein-protein interaction network which revealed that the p53 signaling pathway and cell cycle pathway were two major hubs containing most of the proteins regulated by miR-34a;Studies have demonstrated that miR-34a which is a direct target of the p53 tumor suppressor gene functions as a tumor suppressor and is associated with the tumor growth and metastasis of various human malignances;Knockdown of oncoprotein E6 expression of human papillomavirus in SiHa and HeLa cells by siRNAs lead to an increased protein level of p53 decreased level of miR-34a as well as reduced Warburg effect;miR-34a is known as a p53 regulated tumor suppressor microRNA in many cancer types;In addition in patients with sufficient tumor tissue we assessed p53 mutations and the methylation status of the MIRN34A gene promoter region and correlated these findings with miR-34a expression; Patients with both p53 mutations and low miR-34a levels had the highest probability of relapse P = 0.001;Particularly miR-34a has been revealed to be a direct transcriptional target of p53 which is frequently mutated in epithelial ovarian carcinomas especially in high grade serous cancer; The aim of this study was to investigate the clinical relevance of mir34a as well as its promoter methylation in a subset of 133 ovarian cancers with a special focus on the p53 mutation status the dualistic type I and type II ovarian cancer model and the different histotypes; The expression of miR-34a was found lower in type II than in type I cancers p = 0.037 in p53 mutated as compared to p53 wild type cancers p = 0.003 and in high grade compared to in low grade cancers p = 0.028; The inverse association between miR-34a expression and grading p53 mutation status and dualistic tumor type classification together with its prognostic relevance may underline the tumor-suppressive character of miR-34a in ovarian cancer;As a direct target gene of p53 miR-34a has been suggested to mediate the tumor suppressor function of p53;Further studies indicated that PEG4000-TQ-Nps could significantly increase the expression of miR-34a through p53;Downregulation of miR 34a in breast tumors is not associated with either p53 mutations or promoter hypermethylation while it correlates with metastasis; Recent studies have shown that p53 upregulates miR-34 family leading to direct repression of several key oncogenes; In this study expression of mature miR-34a in breast tumors with wild-type p53 was investigated in order to find any correlation between dysregulation of miR-34a expression and breast cancer; In about 40 % of the wild-type p53 samples miR-34a was significantly downregulated; This study has provided evidence that miR-34a expression can be affected in a significant proportion of breast tumors independent of p53; Knowledge of miR-34a status may provide additional useful information regarding the nature of breast tumors especially when p53 testing does not show any aberration;Among these we found well studied molecules such as the miR-17-92 cluster comprising potent oncogenic microRNA and miR-34 recently found to interact with p53;The results demonstrated that miR-199a and miR-34a could induce the apoptosis of human osteosarcoma cells via p53 signalling pathway;Here we show through expression analysis that miR-34a a p53 target was underexpressed in CD44+ prostate cancer cells purified from xenograft and primary tumors;Members of the miR-34 family have been shown to be transcriptional targets of the tumour suppressor gene P53;Functional genomic analysis highlighted a novel regulatory role of the transcription factor MAZ apart from the known control by p53 on the expression of miR-34a and a number of miR-34a targets; Our analysis for regulatory loops suggest that MAZ and p53 transcription factors co-operate in modulating miR-34a as well as miR-34a targets involved in several cellular pathways;Restoration of tumor suppressor miR 34 inhibits human p53 mutant gastric cancer tumorspheres; MicroRNA miR-34 was recently found to be a direct target of p53 functioning downstream of the p53 pathway as a tumor suppressor; Our results demonstrate that in p53-deficient human gastric cancer cells restoration of functional miR-34 inhibits cell growth and induces chemosensitization and apoptosis indicating that miR-34 may restore p53 function;miR 34 cooperates with p53 in suppression of prostate cancer by joint regulation of stem cell compartment; The miR-34 family was originally found to be a direct target of p53 and is a group of putative tumor suppressors; Here we report that mice with prostate epithelium-specific inactivation of mir-34 and p53 show expansion of the prostate stem cell compartment and develop early invasive adenocarcinomas and high-grade prostatic intraepithelial neoplasia whereas no such lesions are observed after inactivation of either the mir-34 or p53 genes alone by 15 months of age; Consistently combined deficiency of p53 and miR-34 leads to acceleration of MET-dependent growth self-renewal and motility of prostate stem/progenitor cells; Our study provides direct genetic evidence that mir-34 genes are bona fide tumor suppressors and identifies joint control of MET expression by p53 and miR-34 as a key component of prostate stem cell compartment regulation aberrations in which may lead to cancer;The miR-34 family is directly transactivated by tumor suppressor p53 which is frequently mutated in various cancers; however the effect of miR-34a on the ovarian cancer cells remains unclear;The microRNA-34 family miR-34a -34b and -34c have been reported to be tumor suppressor microRNAs miRNAs that are regulated by the TP53 and DNA hypermethylation; To elucidate the roles of miR-34 family in colon carcinogenesis miR-34a/b/c were measured in tumors and adjacent noncancerous tissues from 159 American and 113 Chinese colon cancer patients using quantitative RT-PCR and we examined associations between miR-34a/b/c expression with TNM staging cancer-specific mortality TP53 mutation status and Affymetrix microarray data;Transcription of the three miRNA miR-34 family members was recently found to be directly regulated by p53; Our results demonstrate that miR-34 may restore at least in part the tumor suppressing function of the p53 in p53-deficient human pancreatic cancer cells;p53 status was not correlated with miR-34a;The above results suggest that microRNA-34a is one of the important components of PRIMA-1-induced apoptotic network in the cancer cells harboring mutant p53;MicroRNA-34a miR-34a is a transcriptional target of p53 and is down-regulated in pancreatic cancer;Phytochemical regulation of the tumor suppressive microRNA miR 34a by p53 dependent and independent responses in human breast cancer cells; The tumor suppressive microRNA miR-34a is transcriptionally regulated by p53 and shown to inhibit breast cancer cell proliferation as well as being a marker of increased disease free survival; Human breast cancer cells expressing wild-type MCF-7 or mutant p53 T47D were treated with a concentration range and time course of each phytochemical under conditions of cell cycle arrest as detected by flow cytometry to examine the potential connection between miR-34a expression and their anti-proliferative responses; Our results suggest that miR-34a is an essential component of the anti-proliferative activities of I3C artemisinin and artesunate and demonstrate that both wild-type p53 dependent and independent pathways are responsible for miR-34a induction;Compared with p53 normal group the expression level of miR-34a was significantly lower in p53 deletion group;miR-34a is directly regulated by p53 and acts as tumor suppressor while miR-125b plays a significant role in immune response and apoptosis;The microRNA miR-34 family is a direct transcriptional target of tumor-suppressor TP53 and loss of miR-34 function may impair TP53-mediated cell cycle arrest and apoptosis;It appears that AR-dependent inhibition of p53 resulted in suppression of miR-34a and -34c expression;In this study we evaluated the cascade of events determined by etoposide-induced DNA damage in OS cell lines with different p53 status focusing on methylation status and expression of miR-34a that modulate tumor cell growth and cell cycle progression; Our results suggest that the open and unmethylated conformation of the miR-34a gene may be regulated by p53 able to bind the gene promoter;The miR-34 family under-expressed in-non small cell lung cancers NSCLCs are effectors of p53 activation upon irradiation of cells;MiR-34a a direct p53 target gene possesses tumor-suppressive properties as they mediate apoptosis cell cycle arrest and senescence;The miR-34 family is directly transactivated by tumor suppressor p53 which is frequently mutated in human epithelial ovarian cancer EOC; miR-34a expression is decreased in 100% and miR-34b*/c in 72% of EOC with p53 mutation whereas miR-34a is also downregulated in 93% of tumors with wild-type p53; Finally miR-34 reconstitution experiments in p53 mutant EOC cells resulted in reduced proliferation motility and invasion the latter of which was dependent on MET expression;miR-34a is transcriptionally induced by the tumor suppressor gene p53 which is often downregulated in non-small cell lung cancer NSCLC;In conclusion overexpression of PEBP4 reduced the sensitivity of A549 cells to DDP-induced cytotoxicity mainly through the altered expression of the p53 protein or the modulation of miR-34a;To investigate the effects of miR-449 and miR-34 on cell growth cell cycle and target gene expression based on these miRNA different expressions in ovarian cancer cell lines SKOV3 and SKOV3-ipl both with mutation of p53;Numerous studies have focused on the association between miR-34 family members which are direct p53 targets and carcinogenesis of many cancers including hepatocellular carcinoma HCC;p53 regulates nuclear GSK 3 levels through miR 34 mediated Axin2 suppression in colorectal cancer cells;MicroRNA-34a miR-34a a potential key effector of the p53 tumor-suppressor gene was studied as a potential tumor suppressor in uveal melanoma;The miR-34 family members are direct transcriptional targets of tumor suppressor p53 and loss of miR-34 function can impair p53-mediated cell cycle arrest and apoptosis;Profiling microRNA miRNA expression delineated TP53 alteration-associated miRNA profiles and identified miR-34a and miR-100 as the most significantly down- and upregulated miRNA respectively; Clinically low miR-34a expression and TP53 alterations predicted for chemotherapy resistance and inferior outcome; Thus detailed molecular profiling links impaired p53 to decreased miR-34a expression but also identifies p53-independent miR-34a induction mechanisms as shown in TP53biallelic altered cell lines treated with 15-deoxy-Δ1214-prostaglandin;MiR-34a a direct target of p53 has been shown to target several molecules associated with the cell cycle and cell survival pathways and its dysregulation is implicated in cancer drug resistance or sensitivity in several human cancers;MicroRNA-34a miR-34a is a direct transcriptional target of p53 and links tumor suppressor function and the oncogenic pathways in some cancers;Tumor suppressor p53 transcriptionally regulates expression of microRNA-34a which confers translational inhibition and mRNA degradation of genes involved in cell cycle control and apoptosis; MiR-34a expression was markedly reduced in p53-null PC3 cells and p53-mutated DU145 cells compared with LNCaP cells expressing wild-type p53;The microRNA encoding genes miR-34a and miR-34b/c represent direct p53 target genes and possess tumor suppressive properties as they mediate apoptosis cell cycle arrest and senescence; In the colorectal cancer samples a statistically significant correlation of miR-34a methylation and the absence of p53 mutation was detected; The mutual exclusiveness of miR-34a methylation and p53 mutation indicates that miR-34a inactivation may substitute for loss of p53 function in cancer	;;;;;poor survival;;;malignant trasformation;;;metastasis;;metastasis;;drug resistance;poor survival;;metastasis;;;;;;;metastasis;;;;;;;motility;;staging;tumorigenesis;;;;;drug resistance;poor survival;;immune resistance;;;progression;;;motility;;;;tumorigenesis;;;;drug resistance;poor survival;drug resistance;;;	glioblastoma;glioblastoma;bladder cancer;breast cancer;lung squamous cell cancer;bladder cancer;esophageal cancer;lung squamous cell cancer;melanoma;retinoblastoma;breast cancer;colorectal cancer;colon cancer;colorectal cancer;lung cancer;breast cancer;lung squamous cell cancer;liver cancer;sarcoma;cervical and endocervical cancer;lung squamous cell cancer;lung squamous cell cancer;ovarian cancer;sarcoma;breast cancer;breast cancer;head and neck cancer;sarcoma;prostate cancer;kidney renal cell cancer;breast cancer;gastric cancer;prostate cancer;ovarian cancer;colon cancer;pancreatic cancer;esophageal cancer;lung cancer;pancreatic cancer;breast cancer;B cell lymphoma;cervical and endocervical cancer;colorectal cancer;prostate cancer;sarcoma;lung squamous cell cancer;esophageal cancer;ovarian cancer;lung squamous cell cancer;lung cancer;ovarian cancer;liver cancer;colorectal cancer;melanoma;liver cancer;acute myeloid leukemia;liver cancer;gastric cancer;prostate cancer;sarcoma
hsa-miR-380-5p	TP53	0.356387125389105	0.0163515117264037	-0.346312114104129	1.42081328137354e-05	miRNAWalker2_validate	-0.130032370502874	2.53621800466177e-09		NA	NA	NA
hsa-miR-381-3p	TP53	0.192118086401452	0.203198554750038	-0.346312114104129	1.42081328137354e-05	MirTarget	-0.10958470195975	2.36383687034549e-07		NA	NA	NA
hsa-miR-421	TP53	0.171573235029884	0.0518112933650958	-0.346312114104129	1.42081328137354e-05	miRanda	-0.12756767272718	0.000455424352559313		NA	NA	NA
hsa-miR-491-5p	TP53	0.749881113074991	8.22859263178918e-09	-0.346312114104129	1.42081328137354e-05	MirTarget;miRanda	-0.210461133541589	1.59624493209635e-19	23519249	Targeted site prediction indicated that both Bcl-XL and TP53 contain miR-491-5p recognizing sites in their 3' UTRs; Overexpression of miR-491-5p in the pancreatic cancer cell line SW1990 effectively inhibited both endogenous Bcl-XL and TP53 gene expressions		pancreatic cancer
hsa-miR-504-5p	TP53	0.510726779625117	6.12122269907376e-05	-0.346312114104129	1.42081328137354e-05	miRNAWalker2_validate;MirTarget	-0.175599590135581	1.78517568542536e-12	25015107	TFF1 activates p53 through down regulation of miR 504 in gastric cancer; Alternatively we found that the reconstitution of TFF1 down-regulates miR-504 a negative regulator of p53; Western blot analysis data demonstrated that miR-504 abrogates TFF1-induced p53 protein expression and activity; In conclusion the in vitro and in vivo data demonstrate for the first time a novel mechanism by which the tumor suppressor functions of TFF1 involve activation of p53 through down-regulation of miR-504		gastric cancer
hsa-miR-138-5p	TP73	0.61608764992087	1.35200027885651e-05	-0.964090476895587	5.59044169933305e-09	MirTarget	-0.234483508402263	5.94793628771871e-06		NA	NA	NA
hsa-miR-138-5p	TPM4	0.61608764992087	1.35200027885651e-05	-0.436047146922176	1.13662915419365e-11	miRNATAP	-0.11462005211408	6.87512386989392e-13		NA	NA	NA
hsa-miR-138-5p	TRAM1	0.61608764992087	1.35200027885651e-05	-0.219249743549408	6.52057084378379e-05	MirTarget;miRNATAP	-0.111463208166806	1.46209024045544e-17		NA	NA	NA
hsa-miR-138-5p	TRAM2	0.61608764992087	1.35200027885651e-05	-0.477501519025737	8.94446855861215e-11	mirMAP	-0.161803535839331	6.31810396604652e-14		NA	NA	NA
hsa-miR-138-5p	TRIOBP	0.61608764992087	1.35200027885651e-05	-0.147441285271851	0.00203608986699772	mirMAP	-0.112892443655483	1.36465766006713e-25		NA	NA	NA
hsa-miR-138-5p	VIM	0.61608764992087	1.35200027885651e-05	-0.723805060907832	7.98331283128927e-07	miRNAWalker2_validate	-0.321195743073257	2.27700846705118e-14	26796277;27049260	miR-138 overexpression also down-regulated vimentin expression and upregulated E-cadherin expression suggesting that miR-138 inhibited EMT;In addition the epithelial-mesenchymal transition EMT related markers E-cadherin or vimentin was up-regulated or down-regulated upon the overexpression of miR-138 in NSCLC cells	;	breast cancer;lung squamous cell cancer
hsa-miR-138-5p	ZFP36L2	0.61608764992087	1.35200027885651e-05	-0.383760120585957	4.15502847929805e-07	MirTarget;miRNATAP	-0.236610398696572	4.76362118337576e-35		NA	NA	NA