miRNA gene miRNA_log2FC miRNA_pvalue gene_log2FC gene_pvalue interactions correlation_beta correlation_pvalue PMID evidence outcome cancer hsa-let-7b-5p ABL1 0.604314269683977 0.00140009936153214 -1.32037015957096 1.87647767985755e-18 miRNAWalker2_validate -0.231253752376574 6.2902850853714e-09 NA NA NA hsa-miR-149-5p ABL1 2.94200492826326 4.93436498919036e-14 -1.32037015957096 1.87647767985755e-18 miRNAWalker2_validate -0.143502376394447 3.49799913508757e-15 NA NA NA hsa-miR-484 ABL1 1.81844463411787 1.82951571230938e-15 -1.32037015957096 1.87647767985755e-18 miRNAWalker2_validate -0.280122803941197 1.14978159043687e-19 NA NA NA hsa-miR-181a-5p ATM 2.29556023480783 1.8138457900616e-21 -0.694304374354523 1.11905560067279e-05 miRNAWalker2_validate;miRTarBase -0.126923788457429 2.84207726303723e-05 24531888;27150990;21102523;26113450;23656790 Ataxia-telangiectasia mutation ATM was predicted as a target gene of miR-181a with bioinformatics analysis and was verified by lucifersae reporter assay; A luciferase reporter assay demonstrated that ATM was a direct target of miR-181a miR-181a mimics transfection down regulated ATM mRNA and protein expression; There was inverse correlation between miR-181a and ATM protein expression in gastric cancer and normal gastric tissues; Our study demonstrates that over-expression of miR-181a might be involved in development of gastric cancer by promoting proliferation and inhibiting apoptosis probably through directly targeting ATM miR-181a modulation may be a potential strategy for the development of miRNA-based therapy of gastric cancer;MiR 181a Promotes Proliferation of Human Acute Myeloid Leukemia Cells by Targeting ATM; Dual luciferase reporter gene assay showed that miR-181a significantly suppressed the reporter gene activity containing ATM 3'-UTR by about 56.8% P < 0.05 but it didn't suppress the reporter gene activity containing 3'-UTR ATM mutation; Western blot showed that miR-181a significantly downregulated the expression of ATM in human leukemia cells; It is also found that miR-181a was significantly increased in AML which showed a negative correlation with ATM expression; miR-181a promotes cell proliferation in AML by regulating the tumor suppressor ATM thus it plays the role as oncogene in pathogenesis of AML;Ataxia telangiectasia mutated ATM a target gene of miR-181 exhibited reduced expression in mammospheres and upon TGF-β treatment;miR 181a promotes G1/S transition and cell proliferation in pediatric acute myeloid leukemia by targeting ATM; Pediatric AML patients and healthy controls were enrolled and the expression of miR-181a and ataxia telangiectasia mutated ATM in tissues were examined using quantitative PCR; Moreover cell proliferation and cell cycle were evaluated in several cell lines HL60 NB4 and K562 by using flow cytometry after transfected with miR-181a mimics and inhibitors or ATM siRNA and control siRNA; Finally ATM as the potential target protein of miR-181a was examined; We found that miR-181a was significantly increased in pediatric AML which showed an inverse association with ATM expression; Luciferase activity of the reporter construct identified ATM as the direct molecular target of miR-181a; The results revealed novel mechanism through which miR-181a regulates G1/S transition and cell proliferation in pediatric AML by regulating the tumor suppressor ATM providing insights into the molecular mechanism in pediatric AML;We report that miR-181a and miR-181b were overexpressed in more aggressive breast cancers and their expression correlates inversely with ATM levels ;;;; gastric cancer;acute myeloid leukemia;breast cancer;acute myeloid leukemia;breast cancer hsa-miR-18a-5p ATM 3.78535678765353 3.72446596213886e-26 -0.694304374354523 1.11905560067279e-05 miRNAWalker2_validate;miRTarBase -0.132647027735553 2.53006799595493e-10 23437304;25963391;23857602;23229340 MicroRNA 18a attenuates DNA damage repair through suppressing the expression of ataxia telangiectasia mutated in colorectal cancer; Through in silico search the 3'UTR of Ataxia telangiectasia mutated ATM contains a conserved miR-18a binding site; Expression of ATM was down-regulated in CRC tumors p<0.0001 and inversely correlated with miR-18a expression r = -0.4562 p<0.01; This was further confirmed by the down-regulation of ATM protein by miR-18a; As ATM is a key enzyme in DNA damage repair we evaluated the effect of miR-18a on DNA double-strand breaks; miR-18a attenuates cellular repair of DNA double-strand breaks by directly suppressing ATM a key enzyme in DNA damage repair;However the upregulation of miR-18a suppressed the level of ataxia-telangiectasia mutated and attenuated DNA double-strand break repair after irradiation which re-sensitized the cervical cancer cells to radiotherapy by promoting apoptosis;Furthermore we used antisense oligonucleotides against micro RNAs miRNA or miRNA overexpression plasmids to study the role of miR-18a and -106a on ATM expression; Furthermore we identified that ERα activates miR-18a and -106a to downregulate ATM expression; We reveal a novel mechanism involving ERα and miR-18a and -106a regulation of ATM in breast cancer;MicroRNA 18a upregulates autophagy and ataxia telangiectasia mutated gene expression in HCT116 colon cancer cells; Previous studies showed that certain microRNAs including miR-18a potentially regulate ATM in cancer cells; However the mechanisms behind the modulation of ATM by miR-18a remain to be elucidated in colon cancer cells; In the present study we explored the impact of miR-18a on the autophagy process and ATM expression in HCT116 colon cancer cells; Western blotting and luciferase assays were implemented to explore the impact of miR-18a on ATM gene expression in HCT116 cells; Moreover miR-18a overexpression led to the upregulation of ATM expression and suppression of mTORC1 activity; Results of the present study pertaining to the role of miR-18a in regulating autophagy and ATM gene expression in colon cancer cells revealed a novel function for miR-18a in a critical cellular event and on a crucial gene with significant impacts in cancer development progression treatment and in other diseases ;;;progression colorectal cancer;cervical and endocervical cancer;breast cancer;colon cancer hsa-miR-19b-3p ATM 2.49529833021187 1.57028265846699e-23 -0.694304374354523 1.11905560067279e-05 miRNAWalker2_validate -0.169669050219426 4.03808006538527e-09 NA NA NA hsa-miR-92a-3p ATM 2.06460102658973 1.44784291084757e-19 -0.694304374354523 1.11905560067279e-05 miRNAWalker2_validate -0.174566583478402 5.02119051710453e-08 NA NA NA hsa-miR-335-5p CCNA1 1.77247705492746 2.22457658872091e-06 -0.799524339575412 0.295283787863684 miRNAWalker2_validate -0.252904547371949 0.0095171880094844 NA NA NA hsa-miR-23b-3p CCNB2 -0.251132426825047 0.150200321210792 3.44127671644327 6.15726356293966e-31 miRNAWalker2_validate -0.35472868706084 7.95902161675979e-05 NA NA NA hsa-miR-106b-5p CCND1 2.46782146831112 1.36171495805632e-23 0.0828319966762319 0.840332435689448 miRNAWalker2_validate;miRTarBase -0.190269381519641 0.0130099591661973 NA NA NA hsa-miR-15b-5p CCND1 1.57112623124278 9.14247846750597e-13 0.0828319966762319 0.840332435689448 miRNAWalker2_validate;miRTarBase -0.2743592470705 0.00190316455907807 NA NA NA hsa-miR-195-5p CCND1 -1.44753678070504 8.70594292149271e-09 0.0828319966762319 0.840332435689448 miRNAWalker2_validate;miRTarBase -0.232938095379387 0.00278406868271715 21350001;26631043;25823925 Raf-1 and Ccnd1 were identified as novel direct targets of miR-195 and miR-497 miR-195/497 expression levels in clinical specimens were found to be correlated inversely with malignancy of breast cancer;MiR 195 inhibits the proliferation of human cervical cancer cells by directly targeting cyclin D1; The present study was to evaluate the level of miR-195 and cyclin D1 in CC tissues and cells; We further investigated the molecular mechanisms of miR-195 and cyclin D1 in CC cell lines HeLa and SiHa; Furthermore the expression of miR-195 was inversely proportional to that of cyclin D1 mRNA or protein p = 0.013 p = 0.015 respectively; However the inhibitor of miR-195 promoted the expression of cyclin D1 and cell proliferation; In conclusion our data suggest that miR-195 may have the potential role in treatment of CC patients as well as miR-195 is a novel regulator of invasiveness and tumorigenicity in CC cells by targeting cyclin D1;MicroRNA profiling identifies MiR 195 suppresses osteosarcoma cell metastasis by targeting CCND1; Meanwhile CCND1 was identified as the target gene of miR-195 and further studied; More importantly using real-time PCR we evaluated the expression of miR-195 and CCND1 in osteosarcoma samples from 107 frozen biopsy tissues and 99 formalin- or paraformalin-fixed paraffin-embedded FFPE tissues; Results indicated lowly expressed miR-195 or highly CCND1 correlated with positive overall survival and their expression inversely related to each other; In summary our study suggests miR-195 functions as a tumor metastasis suppressor gene by down-regulating CCND1 and can be used as a potential target in the treatment of osteosarcoma ;;metastasis;poor survival breast cancer;cervical and endocervical cancer;sarcoma hsa-miR-19a-3p CCND1 3.42309334186656 3.02671914353412e-28 0.0828319966762319 0.840332435689448 miRNAWalker2_validate;miRTarBase -0.129855568478024 0.0302697285085785 25985117 Moreover miR-19a might play inhibitory roles in HCC malignancy via regulating Cyclin D1 expression liver cancer hsa-miR-19b-1-5p CCND1 2.57951428759379 4.31576118703427e-20 0.0828319966762319 0.840332435689448 miRNAWalker2_validate;miRTarBase -0.152456226657987 0.0285260627618516 NA NA NA hsa-miR-338-3p CCND1 0.453166438193782 0.144583389707558 0.0828319966762319 0.840332435689448 miRNAWalker2_validate;miRTarBase -0.14528834655399 0.0235908904377559 NA NA NA hsa-miR-365a-3p CCND1 -0.0388985816963467 0.859114494267351 0.0828319966762319 0.840332435689448 miRNAWalker2_validate;miRTarBase -0.20916008203635 0.0224869632381042 NA NA NA hsa-miR-374b-5p CCND1 0.0654362503857184 0.722673188879465 0.0828319966762319 0.840332435689448 miRNAWalker2_validate -0.416222074203323 0.000132219455740898 NA NA NA hsa-miR-92a-3p CCND1 2.06460102658973 1.44784291084757e-19 0.0828319966762319 0.840332435689448 miRNAWalker2_validate -0.18696336621808 0.0257330648039561 NA NA NA hsa-let-7a-5p CCND2 0.618599506841644 2.76973453058748e-05 -2.42747067684236 2.06814828958882e-10 miRNAWalker2_validate;miRTarBase;TargetScan -0.503238938401113 9.92586197811674e-05 20418948 MicroRNA let 7a inhibits proliferation of human prostate cancer cells in vitro and in vivo by targeting E2F2 and CCND2 prostate cancer hsa-let-7b-5p CCND2 0.604314269683977 0.00140009936153214 -2.42747067684236 2.06814828958882e-10 miRNAWalker2_validate;miRTarBase -0.372644945722985 0.000202758514128247 NA NA NA hsa-miR-106b-5p CCND2 2.46782146831112 1.36171495805632e-23 -2.42747067684236 2.06814828958882e-10 miRNAWalker2_validate;miRTarBase -0.723802321113981 4.62852843641777e-26 NA NA NA hsa-miR-141-3p CCND2 5.02396127982626 2.19224509139725e-24 -2.42747067684236 2.06814828958882e-10 TargetScan -0.336824974322951 8.46453268716016e-23 NA NA NA hsa-miR-15a-5p CCND2 2.34669284378787 1.69544424500258e-23 -2.42747067684236 2.06814828958882e-10 miRNAWalker2_validate;miRTarBase -0.558385276567589 5.78612617845985e-14 NA NA NA hsa-miR-16-5p CCND2 1.75824877145857 1.68592440033108e-16 -2.42747067684236 2.06814828958882e-10 miRNAWalker2_validate -0.624880555696101 7.5948593080299e-14 NA NA NA hsa-miR-17-5p CCND2 3.2710598467455 9.93128340539455e-27 -2.42747067684236 2.06814828958882e-10 miRNAWalker2_validate;miRTarBase;TargetScan -0.576586035201243 5.39762569803648e-26 NA NA NA hsa-miR-182-5p CCND2 3.53923166221814 5.07781258121574e-21 -2.42747067684236 2.06814828958882e-10 miRNAWalker2_validate;miRTarBase -0.418107303561313 5.83833309647385e-20 NA NA NA hsa-miR-19b-3p CCND2 2.49529833021187 1.57028265846699e-23 -2.42747067684236 2.06814828958882e-10 miRNAWalker2_validate -0.644240893236217 5.93065810659583e-21 NA NA NA hsa-miR-20a-5p CCND2 3.15577933619191 4.19753346442454e-25 -2.42747067684236 2.06814828958882e-10 miRNAWalker2_validate;miRTarBase -0.552675029838617 1.98133209896024e-23 NA NA NA hsa-miR-301a-3p CCND2 2.81024345929638 2.29784847962242e-17 -2.42747067684236 2.06814828958882e-10 miRNAWalker2_validate -0.490714440601798 1.13987935585442e-18 NA NA NA hsa-miR-320a CCND2 0.438165828017084 0.0390159073347133 -2.42747067684236 2.06814828958882e-10 miRNAWalker2_validate -0.366959333753783 3.90012764364419e-05 NA NA NA hsa-miR-324-3p CCND2 2.08739139768981 3.11885987067952e-13 -2.42747067684236 2.06814828958882e-10 miRNAWalker2_validate -0.569926030100518 1.57078270718816e-20 NA NA NA hsa-miR-335-5p CCND2 1.77247705492746 2.22457658872091e-06 -2.42747067684236 2.06814828958882e-10 miRNAWalker2_validate -0.196309653133352 7.59470226154717e-05 NA NA NA hsa-miR-378a-3p CCND2 -0.10995720000828 0.716188270032681 -2.42747067684236 2.06814828958882e-10 miRNAWalker2_validate -0.264766627168263 2.14263562743039e-05 NA NA NA hsa-miR-423-5p CCND2 0.963563145758616 9.86109015204915e-07 -2.42747067684236 2.06814828958882e-10 miRNAWalker2_validate -0.681308347713645 2.78087673863117e-13 NA NA NA hsa-miR-877-5p CCND2 2.94916202082736 1.8151927276044e-13 -2.42747067684236 2.06814828958882e-10 miRNAWalker2_validate -0.361363420346396 6.83899428438154e-13 NA NA NA hsa-miR-96-5p CCND2 4.89433085814374 1.92000659886961e-31 -2.42747067684236 2.06814828958882e-10 TargetScan -0.382951897231727 7.25785958201884e-21 NA NA NA hsa-miR-27b-3p CCND3 0.196007704287769 0.295630157035388 0.142518749044219 0.397307080616203 miRNAWalker2_validate -0.133645004740845 0.00231237621077374 NA NA NA hsa-miR-23b-3p CDC20 -0.251132426825047 0.150200321210792 3.88984891303216 1.21088023421357e-31 miRNAWalker2_validate -0.444513507865143 9.49371726362108e-06 NA NA NA hsa-miR-30a-5p CDC20 -0.878357906436456 0.000509952992366057 3.88984891303216 1.21088023421357e-31 miRNAWalker2_validate -0.143618820789461 0.0368813303219935 NA NA NA hsa-let-7a-5p CDC25B 0.618599506841644 2.76973453058748e-05 0.783166040527924 0.00478680511553999 miRNAWalker2_validate -0.202803116762794 0.0287409049855185 NA NA NA hsa-miR-141-3p CDC25B 5.02396127982626 2.19224509139725e-24 0.783166040527924 0.00478680511553999 TargetScan -0.118085231335799 3.69707768792997e-06 NA NA NA hsa-miR-23b-3p CDK2 -0.251132426825047 0.150200321210792 0.937881089752417 5.53579780631165e-08 miRNAWalker2_validate -0.108170361258168 0.0284026530581814 NA NA NA hsa-miR-103a-3p CDK6 1.44083190496858 1.53799939616416e-13 -0.774202349805119 0.064787030605636 miRNAWalker2_validate -0.738308002788887 9.81610683337994e-14 NA NA NA hsa-miR-107 CDK6 1.30977326593435 1.30372468603965e-11 -0.774202349805119 0.064787030605636 miRNAWalker2_validate;miRTarBase -0.535825292120497 1.58523365512466e-07 19407485;22491216;21264532;19688090 Enforced expression of miR-107 in MiaPACA-2 and PANC-1 cells downregulated in vitro growth and this was associated with repression of the putative miR-107 target cyclin-dependent kinase 6 thereby providing a functional basis for the epigenetic inactivation of this miRNA in pancreatic cancer;Levels of known miR-107 targets protein kinase Cε PKCε cyclin-dependent kinase 6 CDK6 and hypoxia-inducible factor 1-β HIF1-β decreased following NP/pre-miR-107 treatment;We have identified miR-107 as a potential regulator of CDK6 expression; A bioinformatics search revealed a putative target site for miR-107 within the CDK6 3' untranslated region; Expression of miR-107 in gastric cancer cell lines was found inversely correlated with CDK6 expression; miR-107 could significantly suppress CDK6 3' UTR luciferase reporter activity and this effect was not detectable when the putative 3' UTR target site was mutated; Consistent with the results of the reporter assay ectopic expression of miR-107 reduced both mRNA and protein expression levels of CDK6 inhibited proliferation induced G1 cell cycle arrest and blocked invasion of the gastric cancer cells; Our results suggest that miR-107 may have a tumor suppressor function by directly targeting CDK6 to inhibit the proliferation and invasion activities of gastric cancer cells;Using miRNA-target prediction analyses and the array data we listed up a set of likely targets of miR-107 and miR-185 for G1 cell cycle arrest and validate a subset of them using real-time RT-PCR and immunoblotting for CDK6 ;;; pancreatic cancer;head and neck cancer;gastric cancer;lung squamous cell cancer hsa-miR-141-3p CDK6 5.02396127982626 2.19224509139725e-24 -0.774202349805119 0.064787030605636 TargetScan -0.280860480145549 9.29496321423746e-14 NA NA NA hsa-miR-16-5p CDK6 1.75824877145857 1.68592440033108e-16 -0.774202349805119 0.064787030605636 miRNAWalker2_validate;miRTarBase -0.211183753760106 0.0224108751050014 NA NA NA hsa-miR-17-5p CDK6 3.2710598467455 9.93128340539455e-27 -0.774202349805119 0.064787030605636 TargetScan -0.168193833076577 0.00702167500067962 NA NA NA hsa-miR-185-5p CDK6 2.34016206907488 1.17481626642022e-26 -0.774202349805119 0.064787030605636 miRNAWalker2_validate -0.418001590004214 1.44577313582161e-06 19688090 Using miRNA-target prediction analyses and the array data we listed up a set of likely targets of miR-107 and miR-185 for G1 cell cycle arrest and validate a subset of them using real-time RT-PCR and immunoblotting for CDK6 lung squamous cell cancer hsa-miR-191-5p CDK6 2.30038190670664 9.93191704545938e-17 -0.774202349805119 0.064787030605636 miRNAWalker2_validate;miRTarBase -0.711524835034044 1.00464473356187e-26 NA NA NA hsa-miR-218-5p CDK6 -0.573801507392184 0.0551983860126703 -0.774202349805119 0.064787030605636 miRNAWalker2_validate -0.153512643208175 0.0240408053920225 23996750 Ectopic expression of miR-218 in HepG2 cells resulted in suppressed cell proliferation and enhanced cell apoptosis as well as the down-regulation of Bmi-1 and CDK6 mRNA and protein expressions P<0.05; The low-expression of miR-218 is correlated with malignant clinicopathological characteristics of HCC and miR-218 may inhibit cell proliferation and promote cell apoptosis by down-regulating Bmi-1 and CDK6 in HCC malignant trasformation liver cancer hsa-miR-29b-3p CDK6 1.65828197923813 1.02676780888141e-09 -0.774202349805119 0.064787030605636 miRNAWalker2_validate;miRTarBase -0.224461155748557 0.0022317971289129 23245396;25472644;26180082;23591808;27230400;20086245 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;Here we have identified the oncogene cyclin-dependent protein kinase 6 CDK6 as a direct target of miR-29b in lung cancer;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 ;;;;; melanoma;colorectal cancer;glioblastoma;lung cancer;sarcoma;lymphoma hsa-miR-29c-3p CDK6 -0.00968972577705429 0.97099586346872 -0.774202349805119 0.064787030605636 miRNAWalker2_validate;miRTarBase -0.580639861705711 5.15109801814716e-15 26396669 Furthermore through qPCR and Western blot assays confirmed that overexpression of miR-29c reduced CDK6 mRNA and protein levels; miR-29c could inhibit the proliferation migration and invasion of bladder cancer cells via regulating CDK6 bladder cancer hsa-miR-34a-5p CDK6 1.9016323452565 1.43092834643601e-14 -0.774202349805119 0.064787030605636 miRNAWalker2_validate;miRTarBase -0.519263514540718 3.07288169543583e-11 21702042;26104764 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;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 ; bladder cancer;lung cancer hsa-miR-501-3p CDK6 1.83132758513743 1.10971547702065e-10 -0.774202349805119 0.064787030605636 TargetScan -0.414303056979818 1.84547250783893e-09 NA NA NA hsa-let-7f-5p CDKN1A 0.495648727272215 0.00355972741198794 -1.29236263370998 3.21238784768704e-06 miRNAWalker2_validate -0.24004761105408 0.00296779895445168 NA NA NA hsa-miR-106a-5p CDKN1A 2.48882002962836 1.99757727374521e-12 -1.29236263370998 3.21238784768704e-06 miRNAWalker2_validate;miRTarBase -0.128693729012364 0.000550088861161385 25510666 After prediction with online software we further used dual-luciferase reporter gene assay to ensure that TP53INP1 and CDKN1A might be the direct targets of miR-106a liver cancer hsa-miR-106b-5p CDKN1A 2.46782146831112 1.36171495805632e-23 -1.29236263370998 3.21238784768704e-06 miRNAWalker2_validate;miRTarBase -0.301959313712314 4.48472102839421e-09 NA NA NA hsa-miR-17-5p CDKN1A 3.2710598467455 9.93128340539455e-27 -1.29236263370998 3.21238784768704e-06 miRNAWalker2_validate;miRTarBase;TargetScan -0.172861511846616 3.07251784468708e-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-182-5p CDKN1A 3.53923166221814 5.07781258121574e-21 -1.29236263370998 3.21238784768704e-06 miRNAWalker2_validate -0.109364926293111 0.00141758512280426 NA NA NA hsa-miR-20a-5p CDKN1A 3.15577933619191 4.19753346442454e-25 -1.29236263370998 3.21238784768704e-06 miRNAWalker2_validate;miRTarBase -0.165884225022855 7.19614215488726e-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-20b-5p CDKN1A 2.07706563022469 1.10107236083433e-05 -1.29236263370998 3.21238784768704e-06 miRNAWalker2_validate;miRTarBase -0.112000786094038 7.41332851839187e-05 NA NA NA hsa-miR-28-5p CDKN1A 0.230152919654905 0.0742909586754846 -1.29236263370998 3.21238784768704e-06 miRNAWalker2_validate;miRTarBase -0.556544696034112 2.23374029772338e-07 NA NA NA hsa-miR-335-5p CDKN1A 1.77247705492746 2.22457658872091e-06 -1.29236263370998 3.21238784768704e-06 miRNAWalker2_validate -0.15287461273454 1.73689594092226e-05 NA NA NA hsa-miR-345-5p CDKN1A 3.63532310411307 2.2698112107996e-21 -1.29236263370998 3.21238784768704e-06 miRNAWalker2_validate;miRTarBase -0.214757145120261 7.64097376843956e-11 NA NA NA hsa-miR-363-3p CDKN1A 1.50575300026701 0.00020976164678918 -1.29236263370998 3.21238784768704e-06 miRNAWalker2_validate;miRTarBase -0.119979037678532 0.000289602460917026 NA NA NA hsa-miR-423-3p CDKN1A 2.57855385753676 9.19765570228097e-24 -1.29236263370998 3.21238784768704e-06 miRNAWalker2_validate;miRTarBase -0.200481634838583 5.95960562762572e-05 NA NA NA hsa-miR-503-5p CDKN1A 3.66513190181895 6.60300917645278e-21 -1.29236263370998 3.21238784768704e-06 miRNAWalker2_validate;miRTarBase -0.108479527294966 0.00188268400827089 NA NA NA hsa-miR-505-5p CDKN1A 1.89243395287645 9.82003586561819e-12 -1.29236263370998 3.21238784768704e-06 miRNAWalker2_validate -0.197864415222474 3.15355511624094e-05 NA NA NA hsa-miR-93-5p CDKN1A 3.03961860136032 1.11672209617395e-24 -1.29236263370998 3.21238784768704e-06 miRNAWalker2_validate;miRTarBase -0.230725362813635 6.59990926283075e-08 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-942-5p CDKN1A 2.35195531153712 5.45059325728841e-16 -1.29236263370998 3.21238784768704e-06 miRNAWalker2_validate -0.260648356679274 4.62199208083779e-09 NA NA NA hsa-miR-96-5p CDKN1A 4.89433085814374 1.92000659886961e-31 -1.29236263370998 3.21238784768704e-06 miRNAWalker2_validate;miRTarBase -0.131322885353092 1.73810674264337e-05 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 1.11154309866014 1.24143909012085e-08 -1.29236263370998 3.21238784768704e-06 miRNAWalker2_validate -0.251133283878821 0.000264648620156197 NA NA NA hsa-miR-221-3p CDKN1B 0.451556679024397 0.0909808299917811 0.111589542072177 0.453851218822883 miRNAWalker2_validate;miRTarBase -0.108173416521144 5.5134677794152e-05 23637992;19953484;23939688;19126397;20146005;23967190;17569667;22992757;17721077;20461750 miR-221 knockdown not only blocked cell cycle progression induced cell apoptosis and inhibited cell proliferation in-vitro but it also inhibited in-vivo tumor growth by targeting p27kip1;Based on bioinformatic analysis we found that the seed sequences of miR-221 and miR-222 coincide with each other and p27kip1 is a target for miRNA-221/222;A Slug/miR-221 network has been suggested linking miR-221 activity with the downregulation of a Slug repressor leading to Slug/miR-221 upregulation and p27Kip1 downregulation; Interference with this process can be achieved using antisense miRNA antagomiR molecules targeting miR-221 inducing the downregulation of Slug and the upregulation of p27Kip1;Moreover a series of functional assays demonstrated that mir-221 could directly inhibit cKit p27Kip1 and possibly other pivotal proteins in melanoma;Matched HCC and adjacent non-cancerous samples were assayed for the expression of miR-221 and three G1/S transition inhibitors: p27Kip1 p21WAF1/Cip1and TGF-β1 by in situ hybridization and immunohistochemistry respectively; Real time qRT-PCR was used to investigate miR-221 and p27Kip1 transcripts in different clinical stages; In result miR-221 and TGF-β1 are frequently up-regulated in HCC while p27Kip1 and p21WAF1/Cip1 proteins are frequently down-regulated; In conclusion miR-221 is important in tumorigenesis of HCC possibly by specifically down-regulating p27Kip1 a cell-cycle inhibitor;Additionally the PDGF-dependent increase in cell proliferation appears to be mediated by inhibition of a specific target of miR-221 and down-regulation of p27Kip1;miR 221 and miR 222 expression affects the proliferation potential of human prostate carcinoma cell lines by targeting p27Kip1; In all cell lines tested we show an inverse relationship between the expression of miR-221 and miR-222 and the cell cycle inhibitor p27Kip1; Consistently miR-221 and miR-222 knock-down through antisense LNA oligonucleotides increases p27Kip1 in PC3 cells and strongly reduces their clonogenicity in vitro;Peptide nucleic acids targeting miR 221 modulate p27Kip1 expression in breast cancer MDA MB 231 cells; Targeting miR-221 by PNA resulted in i lowering of the hybridization levels of miR-221 measured by RT-qPCR ii upregulation of p27Kip1 gene expression measured by RT-qPCR and western blot analysis;Antagonism of either microRNA 221 or 222 in glioblastoma cells also caused an increase in p27Kip1 levels and enhanced expression of the luciferase reporter gene fused to the p27Kip1 3'UTR;MiR 221 and MiR 222 alterations in sporadic ovarian carcinoma: Relationship to CDKN1B CDKNIC and overall survival; miR-221 and miR-222 negatively regulate expression of CDKN1B p27 and CDKN1C p57 two cell cycle regulators expressed in ovarian surface epithelium and down-regulated in ovarian carcinomas; In contrast CDKN1B expression was not associated with miR-221 or miR-222 expression progression;;;;staging;tumorigenesis;;;;;poor survival breast cancer;glioblastoma;breast cancer;melanoma;liver cancer;pancreatic cancer;prostate cancer;breast cancer;glioblastoma;ovarian cancer hsa-miR-24-3p CDKN1B 0.99989036772428 1.35595013650376e-07 0.111589542072177 0.453851218822883 miRNAWalker2_validate -0.155773035071718 3.27990988982606e-05 26847530;26044523 The biological significance of miR-24 expression in prostate cancer cells was assessed by a series of in vitro bioassays and the effect on proposed targets p27 CDKN1B and p16 CDK2NA was investigated;With the bioinformatic method we further identified that p27Kip1 is a direct target of miR-24-3p and its protein level was negatively regulated by miR-24-3p ; prostate cancer;breast cancer hsa-miR-221-3p CDKN1C 0.451556679024397 0.0909808299917811 -1.44787932669971 3.93876960323515e-05 miRNAWalker2_validate;miRTarBase -0.248677574564568 0.000109625580592135 20461750 miR-221 and miR-222 negatively regulate expression of CDKN1B p27 and CDKN1C p57 two cell cycle regulators expressed in ovarian surface epithelium and down-regulated in ovarian carcinomas; Higher miR-222 and miR-221 expression were significantly associated with decreased CDKN1C expression P = 0.009 and 0.01 ovarian cancer hsa-miR-222-3p CDKN1C 0.851783756239071 0.00266783568486918 -1.44787932669971 3.93876960323515e-05 miRNAWalker2_validate;miRTarBase -0.245957660234723 4.42600884082533e-05 20461750 miR-221 and miR-222 negatively regulate expression of CDKN1B p27 and CDKN1C p57 two cell cycle regulators expressed in ovarian surface epithelium and down-regulated in ovarian carcinomas; Higher miR-222 and miR-221 expression were significantly associated with decreased CDKN1C expression P = 0.009 and 0.01 ovarian cancer hsa-miR-25-3p CDKN1C 1.36472605225697 4.83790725935681e-11 -1.44787932669971 3.93876960323515e-05 miRNAWalker2_validate;miRTarBase -0.164310296045477 0.0444913812224325 NA NA NA hsa-miR-335-5p CDKN1C 1.77247705492746 2.22457658872091e-06 -1.44787932669971 3.93876960323515e-05 miRNAWalker2_validate -0.104413309854971 0.0214598308380321 NA NA NA hsa-miR-10b-5p CDKN2A -0.155951595811628 0.555006386998027 2.50186258213173 0.00259397623852446 miRNAWalker2_validate;miRTarBase -0.395669711540304 0.0100450205079681 NA NA NA hsa-miR-34a-5p CDKN2C 1.9016323452565 1.43092834643601e-14 0.22688212352847 0.433133415352322 miRNAWalker2_validate -0.218709270480303 6.47001667111707e-05 NA NA NA hsa-miR-23b-3p E2F1 -0.251132426825047 0.150200321210792 2.30029093432361 6.42780154222742e-15 miRNAWalker2_validate -0.372989133559732 1.24396495100595e-05 NA NA NA hsa-miR-125b-5p E2F3 -1.16462950151259 0.000288900271798384 0.864092775291151 0.000386058881687169 miRNAWalker2_validate;miRTarBase -0.142837036867265 9.12438435050649e-05 20549700;22523546 E2F3 which was critical for G1/S transition and was overexpressed in most of poor-differentiated bladder cancers was identified as a target of miR-125b by luciferase assay; Introduction of miR-125b could reduce the expression of E2F3 protein but not the E2F3 mRNA;Moreover we demonstrated that the E2F3 was a direct target of miR-125b in breast cancer cells ; bladder cancer;breast cancer hsa-miR-140-5p EP300 0.844753502512594 3.73722278438606e-05 -0.259813561364416 0.130645976324069 miRNAWalker2_validate -0.116180580124631 0.0041461159891489 NA NA NA hsa-miR-193b-3p EP300 2.25711804611899 4.1940744806631e-14 -0.259813561364416 0.130645976324069 miRNAWalker2_validate -0.105745678811168 8.10977033783005e-05 NA NA NA hsa-miR-374a-5p GADD45A 0.484615721953736 0.0042981729815149 -0.835839078652441 0.000140836693353512 miRNAWalker2_validate;miRTarBase -0.155554493831768 0.0148586446317536 NA NA NA hsa-miR-145-5p HDAC2 -1.55259331973517 9.97889123247165e-07 0.313249438836848 0.0173965895741346 miRNAWalker2_validate -0.114388862244791 4.4414066471407e-09 23499894 MiR 145 functions as a tumor suppressor by directly targeting histone deacetylase 2 in liver cancer; Ectopic expression of miRNA mimics evidenced that miR-145 suppresses HDAC2 expression in HCC cells; In conclusion we suggest that loss or suppression of miR-145 may cause aberrant overexpression of HDAC2 and promote HCC tumorigenesis tumorigenesis liver cancer hsa-let-7f-5p MYC 0.495648727272215 0.00355972741198794 -1.76968865889126 2.71829937908146e-06 miRNAWalker2_validate -0.302610362502413 0.00593577090066522 NA NA NA hsa-let-7g-5p MYC 1.20061455355116 1.50237505511483e-12 -1.76968865889126 2.71829937908146e-06 miRNAWalker2_validate;miRTarBase -0.647634835001101 8.67569135821405e-10 NA NA NA hsa-miR-320a MYC 0.438165828017084 0.0390159073347133 -1.76968865889126 2.71829937908146e-06 miRNAWalker2_validate -0.270203083250914 0.00203008366284758 25736597 Furthermore progesterone P4 promoted the expression of miR-320a by repressing c-Myc expression while estrogen E2 exerted the opposite effect breast cancer hsa-miR-320b MYC 1.55692969039548 1.41071034251915e-08 -1.76968865889126 2.71829937908146e-06 miRNAWalker2_validate -0.211227042104883 0.00142753396089349 26487644 miR 320b suppresses cell proliferation by targeting c Myc in human colorectal cancer cells; Overexpression of miR-320b in CRC cells was statistically correlated with a decrease of cell growth in vitro and in vivo while c-MYC was identified as a target gene of miR-320b in CRC; Furthermore it was found that up-regulation of c-Myc can attenuate the effects induced by miR-320b; Our identification of c-MYC as a target gene of miR-320b provides new insights into the pathophysiology of CRC proliferation and identifies miR-320b as a novel therapeutic target for the treatment of CRC colorectal cancer hsa-miR-335-5p MYC 1.77247705492746 2.22457658872091e-06 -1.76968865889126 2.71829937908146e-06 miRNAWalker2_validate -0.15527675337735 0.00141118517916367 NA NA NA hsa-miR-34a-5p MYC 1.9016323452565 1.43092834643601e-14 -1.76968865889126 2.71829937908146e-06 miRNAWalker2_validate;miRTarBase -0.359767953473847 5.62932761832786e-07 25572695;25686834;21460242;22159222;23640973;22830357;22235332 The c-Myc and CD44 were confirmed as direct targets of miR-34a in EJ cell apoptosis induced by PRE;miR 34a induces cellular senescence via modulation of telomerase activity in human hepatocellular carcinoma by targeting FoxM1/c Myc pathway;Myc mediated repression of microRNA 34a promotes high grade transformation of B cell lymphoma by dysregulation of FoxP1;MicroRNA 34a suppresses malignant transformation by targeting c Myc transcriptional complexes in human renal cell carcinoma; We investigated the functional effects of microRNA-34a miR-34a on c-Myc transcriptional complexes in renal cell carcinoma; miR-34a down-regulated expression of multiple oncogenes including c-Myc by targeting its 3' untranslated region which was revealed by luciferase reporter assays; Our results demonstrate that miR-34a suppresses assembly and function of the c-Myc complex that activates or elongates transcription indicating a novel role of miR-34a in the regulation of transcription by c-Myc;Among them miR-34a was also associated with poor prognosis in 2 independent series of leukemic and nodal MCL and in cooperation with high expression of the MYC oncogene;We report that miR-34a did not inhibit cell proliferation notwithstanding a marked down-regulation of c-MYC;MicroRNA 34a modulates c Myc transcriptional complexes to suppress malignancy in human prostate cancer cells; We studied the functional effects of miR-34a on c-Myc transcriptional complexes in PC-3 prostate cancer cells; miR-34a downregulated expression of c-Myc oncogene by targeting its 3' UTR as shown by luciferase reporter assays; This is the first report to document that miR-34a suppresses assembly and function of the c-Myc-Skp2-Miz1 complex that activates RhoA and the c-Myc-pTEFB complex that elongates transcription of various genes suggesting a novel role of miR-34a in the regulation of transcription by c-Myc complex ;;;malignant trasformation;worse prognosis;; bladder cancer;liver cancer;B cell lymphoma;kidney renal cell cancer;lymphoma;lymphoma;prostate cancer hsa-miR-423-5p MYC 0.963563145758616 9.86109015204915e-07 -1.76968865889126 2.71829937908146e-06 miRNAWalker2_validate -0.592117097378242 1.10389937335588e-10 NA NA NA hsa-miR-429 MYC 4.48815175680773 2.44117492218206e-17 -1.76968865889126 2.71829937908146e-06 miRNAWalker2_validate -0.269400502460394 6.09134482841112e-17 21684154;24633485 miR 429 modulates the expression of c myc in human gastric carcinoma cells; SGC-7901 gastric cancer cells were transfected with miR-429 mimics and endogenous c-myc expression was detected by western blots; We performed functional assays using the 3'UTR of the c-myc gene as a miR-429 target in a luciferase reporter assay system; miR-429 significantly downregulated endogenous c-myc expression in SGC-7901 cells; Action of miR/429 on c-myc 3'UTR was confirmed; c-myc is an important miR-429 target gene;It is known that miR-429 is down-regulated and functions as a tumor suppressor by targeting c-myc and PLGG1 in gastric and breast cancer ; gastric cancer;sarcoma hsa-miR-744-5p MYC 1.48254348878737 3.23019501613577e-09 -1.76968865889126 2.71829937908146e-06 miRNAWalker2_validate -0.254793177391621 0.000439915184612437 24991193 Decrease expression of microRNA 744 promotes cell proliferation by targeting c Myc in human hepatocellular carcinoma; Quantitative reverse-transcription polymerase chain reaction qRT-PCR was conducted to detect the expression of miR-744 and Immunohistochemistry was performed to detect expression of c-Myc in HCC specimens and adjacent normal tissues; Luciferase reporter assays was performed to confirm whether miR-744 regulated the expression of c-Myc; Luciferase assay and Western blot analysis revealed that c-Myc is a direct target of miR-744; Down-regulation of miR-744 and up-regulation of c-Myc were detected in HCC specimens compared with adjacent normal tissues; Moreover restoration of miR-744 rescues c-Myc induced HCC proliferation; Our data suggest that miR-744 exerts its tumor suppressor function by targeting c-Myc leading to the inhibition of HCC cell growth liver cancer hsa-miR-98-5p MYC 1.11154309866014 1.24143909012085e-08 -1.76968865889126 2.71829937908146e-06 miRNAWalker2_validate;miRTarBase -0.602921793997467 5.7325871539819e-11 NA NA NA hsa-miR-106a-5p RB1 2.48882002962836 1.99757727374521e-12 -0.453832349621869 0.0641807656041741 miRNAWalker2_validate;miRTarBase -0.207146169416987 9.29749287107945e-11 NA NA NA hsa-miR-106b-5p RB1 2.46782146831112 1.36171495805632e-23 -0.453832349621869 0.0641807656041741 miRNAWalker2_validate;miRTarBase -0.179483553741754 7.94488434930651e-05 NA NA NA hsa-miR-17-5p RB1 3.2710598467455 9.93128340539455e-27 -0.453832349621869 0.0641807656041741 miRNAWalker2_validate;miRTarBase;TargetScan -0.176683696046635 9.85172436957833e-07 NA NA NA hsa-miR-192-5p RB1 2.69002528723195 1.22990188194432e-16 -0.453832349621869 0.0641807656041741 miRNAWalker2_validate;miRTarBase -0.153739765157225 1.07660617507336e-05 NA NA NA hsa-miR-20a-5p RB1 3.15577933619191 4.19753346442454e-25 -0.453832349621869 0.0641807656041741 miRNAWalker2_validate;miRTarBase -0.177203787298137 1.08156578899176e-06 NA NA NA hsa-miR-93-5p RB1 3.03961860136032 1.11672209617395e-24 -0.453832349621869 0.0641807656041741 miRNAWalker2_validate -0.167206817770783 8.36156887116369e-06 NA NA NA hsa-miR-155-5p SMAD3 1.20164021433135 0.00086170622431261 -0.145068391221315 0.569239559252949 miRNAWalker2_validate -0.167586664196246 6.20173080978562e-07 27626488 Here we demonstrated that TGF-β1 elevated the expression of miR-155 in colorectal cancer cells through SMAD3 and SMAD4 colorectal cancer hsa-miR-18a-5p SMAD3 3.78535678765353 3.72446596213886e-26 -0.145068391221315 0.569239559252949 miRNAWalker2_validate -0.136878014915373 5.63544047470077e-05 23249750 The unexpected effects of miR-18a on CTGF transcription are mediated in part by direct targeting of Smad3 and ensuing weakening of TGFβ signaling glioblastoma hsa-miR-186-5p SMAD4 1.47445398888668 3.0781726595413e-15 -0.586921155134023 3.52416916552263e-06 miRNAWalker2_validate -0.107040467643529 0.000873099593755318 NA NA NA hsa-miR-320a SMC1A 0.438165828017084 0.0390159073347133 0.043831182387617 0.773298330936153 miRNAWalker2_validate -0.123748010459244 0.000360165063457412 NA NA NA hsa-miR-26b-5p STAG1 0.885393662798425 3.2116297961629e-06 -0.245728256557948 0.202447685081763 miRNAWalker2_validate -0.171395587122058 0.000450364078328837 NA NA NA hsa-miR-21-5p STAG2 2.73773305747971 1.38864982139576e-43 -0.338909993805473 0.122578778455043 miRNAWalker2_validate -0.121496795603237 0.0125257945480539 NA NA NA hsa-miR-744-5p TGFB1 1.48254348878737 3.23019501613577e-09 -0.000200257511168367 0.999409206375481 miRNAWalker2_validate -0.229419410482444 6.9384219754003e-06 NA NA NA hsa-miR-141-3p TGFB2 5.02396127982626 2.19224509139725e-24 -1.19931727990522 0.00330886829654418 miRNAWalker2_validate;miRTarBase;TargetScan -0.360699351018386 8.70106540908034e-24 NA NA NA hsa-miR-29b-3p TGFB2 1.65828197923813 1.02676780888141e-09 -1.19931727990522 0.00330886829654418 miRTarBase -0.231729413265765 0.0012231669483933 NA NA NA hsa-miR-335-5p TGFB2 1.77247705492746 2.22457658872091e-06 -1.19931727990522 0.00330886829654418 miRNAWalker2_validate -0.252111592909568 1.14412319370904e-06 NA NA NA hsa-miR-10a-5p TGFB3 1.15016989191194 0.00372037233992369 -1.92191802151593 4.13522948700016e-07 miRNAWalker2_validate -0.418366510356312 7.09740564892359e-21 NA NA NA hsa-miR-29b-3p TGFB3 1.65828197923813 1.02676780888141e-09 -1.92191802151593 4.13522948700016e-07 miRTarBase -0.399950302957701 1.59835018316921e-09 NA NA NA hsa-miR-221-3p TP53 0.451556679024397 0.0909808299917811 0.17313275059387 0.48779406985331 miRNAWalker2_validate -0.115825211031354 0.0105671893909646 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 0.851783756239071 0.00266783568486918 0.17313275059387 0.48779406985331 miRNAWalker2_validate -0.116904656132339 0.00589565055970469 NA NA NA hsa-miR-155-5p WEE1 1.20164021433135 0.00086170622431261 -1.40590862047516 1.76830074250163e-11 miRNAWalker2_validate -0.118659419923154 2.97968064982433e-05 NA NA NA hsa-miR-27a-3p WEE1 1.66542180327138 4.93775737894805e-13 -1.40590862047516 1.76830074250163e-11 miRTarBase -0.149688562062089 0.000640862927163398 NA NA NA hsa-miR-424-5p WEE1 1.61930224569578 1.89642549274994e-10 -1.40590862047516 1.76830074250163e-11 miRNAWalker2_validate;miRTarBase -0.13494137451283 0.000730263963561331 NA NA NA hsa-miR-26a-5p YWHAE 0.0464832722967259 0.752628386912329 0.514491612368612 0.000180862815548893 miRNAWalker2_validate -0.174289033994773 0.000159844329938043 NA NA NA hsa-miR-103a-3p YWHAH 1.44083190496858 1.53799939616416e-13 -0.039384739798634 0.787929142314944 miRNAWalker2_validate -0.161531751525804 4.29697423677565e-06 NA NA NA