miRNA gene miRNA_log2FC miRNA_pvalue gene_log2FC gene_pvalue interactions correlation_beta correlation_pvalue PMID evidence outcome cancer hsa-miR-103a-3p PTEN 1.44083190496858 1.53799939616416e-13 -0.452835975443078 0.00142504206837966 miRNAWalker2_validate;miRTarBase -0.181124200363514 1.1176220548008e-07 26511107;24828205 LncRNA GAS5 induces PTEN expression through inhibiting miR 103 in endometrial cancer cells; To investigate the expression of GAS5 PTEN and miR-103 RT-PCR was performed; Finally we found that miR-103 mimic could decrease the mRNA and protein levels of PTEN through luciferase reporter assay and western blotting and GAS5 plasmid may reverse this regulation effect in endometrial cancer cells; Through inhibiting the expression of miR-103 GAS5 significantly enhanced the expression of PTEN to promote cancer cell apoptosis and thus could be an important mediator in the pathogenesis of endometrial cancer;Our data collectively demonstrate that miR-103 is an oncogene miRNA that promotes colorectal cancer proliferation and migration through down-regulation of the tumor suppressor genes DICER and PTEN ; endometrial cancer;colorectal cancer hsa-miR-106a-5p PTEN 2.48882002962836 1.99757727374521e-12 -0.452835975443078 0.00142504206837966 miRNATAP -0.119115957971973 1.32932348443908e-10 26097565;26318586 miR 106a promotes growth and metastasis of non small cell lung cancer by targeting PTEN; Furthermore the presence of miR-106a was inversely correlated with PTEN in NSCLC tissues; Overall this study suggested that miR-106a inhibited the growth and metastasis of NSCLC cells by decreasing PTEN expression;Further pterostilbene through downregulation of miR-17-5p and miR-106a-5p expression both in tumors and systemic circulation rescued PTEN mRNA and protein levels leading to reduced tumor growth in vivo metastasis; lung squamous cell cancer;prostate cancer hsa-miR-106b-5p PTEN 2.46782146831112 1.36171495805632e-23 -0.452835975443078 0.00142504206837966 miRNAWalker2_validate;miRTarBase;miRNATAP -0.167925855213166 9.91778363511573e-11 24842611;26238857;26722252 MicroRNA 106b in cancer associated fibroblasts from gastric cancer promotes cell migration and invasion by targeting PTEN;We further identified PTEN and p21 as novel direct targets of miR-106b by using target prediction algorithms and a luciferase assay; Overexpression of miR-106b reduced the expression of PTEN and p21 and increased the expression of p-AKT which is a downstream of PTEN; Restoring the expression of PTEN or p21 in stably miR-106b-overexpressed cells could rescue the effect of miR-106b on cell radioresistance; These observations illustrated that miR-106b could induce cell radioresistance by directly targeting PTEN and p21 this process was accompanied by tumour-initiating cell capacity enhancement which is universally confirmed to be associated with radioresistance;Cantharidin modulates the E2F1/MCM7 miR 106b 93/p21 PTEN signaling axis in MCF 7 breast cancer cells cell migration;drug resistance; gastric cancer;colorectal cancer;breast cancer hsa-miR-107 PTEN 1.30977326593435 1.30372468603965e-11 -0.452835975443078 0.00142504206837966 miRNAWalker2_validate;PITA;miRanda -0.125872445510677 0.000311847826997376 NA NA NA hsa-miR-130a-3p PTEN 2.02021855058359 1.26427102520415e-11 -0.452835975443078 0.00142504206837966 MirTarget;miRNATAP -0.107066992505531 1.60679955529776e-06 26837847;24490491;27062783;22614869;27040383;27035216;26043084 The miR 130 family promotes cell migration and invasion in bladder cancer through FAK and Akt phosphorylation by regulating PTEN; In clinical bladder cancer specimens downregulation of PTEN was found to be closely correlated with miR-130 family expression levels;Down-regulated miR-130a did not affect cell proliferations but enhanced the sensitivity of the cells to cisplatin inhibited the expressions of MDR1 mRNA and P-gp and increased the expression of PTEN proteins; MiR-130a inhibitor can reverse the cisplatin resistance by upregulating the expression of PTEN proteins and down-regulating P-gp in A2780 cell lines;Platinum-resistant patients had significantly higher levels of expression of miR-130a and BCL-2 and lower level of PTEN than platinum-sensitive patients P < 0.05; MiR-130a may mediate the generation of platinum resistance in epithelial ovarian cancer through inhibiting PTEN to activate PI3K/AKT signaling pathway and increasing BCL-2 to inhibit tumor cell apoptosis;We found that miR-130a was upregulated in SKOV3/CIS compared to the parental SKOV3 cells and PTEN was predicted to be the potential target of miR-130a;In addition by targeting PTEN 3' untranslated region miR-130a might increase cell growth and initiate protein kinase B AKT pathway activation;MicroRNA 130a promotes the metastasis and epithelial mesenchymal transition of osteosarcoma by targeting PTEN; MiR-130a exerted promoting effects on metastatic behavior and EMT of osteosarcoma cells through suppressing PTEN expression;This role of miR-130a may be achieved by regulating the MDR1 and PTEN gene expression cell migration;drug resistance;drug resistance;;;metastasis; bladder cancer;ovarian cancer;ovarian cancer;ovarian cancer;cervical and endocervical cancer;sarcoma;ovarian cancer hsa-miR-130b-3p PTEN 3.5350292994509 1.73934183852569e-27 -0.452835975443078 0.00142504206837966 MirTarget;miRNATAP -0.118523549020844 1.10168456648735e-09 26837847;25637514 The miR 130 family promotes cell migration and invasion in bladder cancer through FAK and Akt phosphorylation by regulating PTEN; In clinical bladder cancer specimens downregulation of PTEN was found to be closely correlated with miR-130 family expression levels;MiR 130b plays an oncogenic role by repressing PTEN expression in esophageal squamous cell carcinoma cells; We confirmed that miR-130b interacted with the 3'-untranslated region of PTEN and that an increase in the expression level of miR-130b negatively affected the protein level of PTEN; However the dysregulation of miR-130b had no obvious impact on PTEN mRNA; As Akt is a downstream effector of PTEN we explored if miR-130b affected Akt expression and found that miR-130b indirectly regulated the level of phosphorylated Akt while total Akt protein remained unchanged; The results indicate that miR-130b plays an oncogenic role in ESCC cells by repressing PTEN expression and Akt phosphorylation which would be helpful in developing miRNA-based treatments for ESCC cell migration; bladder cancer;esophageal cancer hsa-miR-148a-3p PTEN 1.26728238710376 2.52325607402829e-06 -0.452835975443078 0.00142504206837966 MirTarget;miRNATAP -0.102658849708203 4.6220389940495e-05 22496917 Introduction of anti-miR-148a increased PTEN protein and mRNA expression suggesting that PTEN was targeted by miR-148a liver cancer hsa-miR-148b-3p PTEN 1.97815018171325 6.07715327281595e-26 -0.452835975443078 0.00142504206837966 MirTarget;miRNATAP -0.168985576302433 9.27873273241405e-07 NA NA NA hsa-miR-15b-3p PTEN 2.33847028227712 4.29662877950836e-19 -0.452835975443078 0.00142504206837966 mirMAP -0.110608587315208 9.86982828042873e-06 NA NA NA hsa-miR-16-2-3p PTEN 2.31623086727196 4.29838149388188e-20 -0.452835975443078 0.00142504206837966 mirMAP -0.10224879739163 8.32790317307332e-05 NA NA NA hsa-miR-17-5p PTEN 3.2710598467455 9.93128340539455e-27 -0.452835975443078 0.00142504206837966 miRNAWalker2_validate;miRTarBase;TargetScan;miRNATAP -0.128957385840206 5.08699518968894e-10 27400681;23391506;23133552;26629823;24462867;26318586;26215320;25634356;26500892;24912422;23418359 GFRα2 prompts cell growth and chemoresistance through down regulating tumor suppressor gene PTEN via Mir 17 5p in pancreatic cancer; Mechanically we discovered that high GFRα2 expression level leads to PTEN inactivation via enhancing Mir-17-5p level;We found that these phenotypes were the results of miR-17 targeting PTEN;PTEN mRNA correlated inversely with miR-92a and members of the miR-17 and miR-130/301 families;We hypothesized that knocking down the oncogenic microRNA oncomiR miR-17-5p might restore the expression levels of PDCD4 and PTEN tumor suppressor proteins illustrating a route to oligonucleotide therapy of TNBC; Contrary to conventional wisdom antisense knockdown of oncomiR miR-17-5p guide strand reduced PDCD4 and PTEN proteins by 1.8±0.3 fold in human TNBC cells instead of raising them; Bioinformatics analysis and folding energy calculations revealed that mRNA targets of miR-17-5p guide strand such as PDCD4 and PTEN could also be regulated by miR-17-3p passenger strand;miR 17 inhibitor suppressed osteosarcoma tumor growth and metastasis via increasing PTEN expression; Expression of miR-17 was negatively correlated with PTEN in OS tissues;Resveratrol and pterostilbene epigenetically restore PTEN expression by targeting oncomiRs of the miR 17 family in prostate cancer; Further pterostilbene through downregulation of miR-17-5p and miR-106a-5p expression both in tumors and systemic circulation rescued PTEN mRNA and protein levels leading to reduced tumor growth in vivo;In addition ERβ expression significantly increased in calycosin-treated HCT-116 cells followed by a decrease of miR-17 and up-regulation of PTEN; Our results indicate that calycosin has an inhibitory effect on CRC which might be obtained by ERβ-mediated regulation of miR-17 and PTEN expression;The High Expression of the microRNA 17 92 Cluster and its Paralogs and the Downregulation of the Target Gene PTEN Is Associated with Primary Cutaneous B Cell Lymphoma Progression;MicroRNA 17 5p induces drug resistance and invasion of ovarian carcinoma cells by targeting PTEN signaling; miR-17-5p activates AKT by downregulation of PTEN in ovarian cancer cells;MicroRNA 17 5p promotes chemotherapeutic drug resistance and tumour metastasis of colorectal cancer by repressing PTEN expression; We found that PTEN was a target of miR-17-5p in the colon cancer cells and their context-specific interactions were responsible for multiple drug-resistance; Chemotherapy was found to increase the expression levels of miR-17-5p which further repressed PTEN levels contributing to the development of chemo-resistance; MiR-17-5p is a predictive factor for chemotherapy response and a prognostic factor for overall survival in CRC which is due to its regulation of PTEN expression;The mature miR-17-5p exerted this function by repressing the expression of PTEN drug resistance;;;;metastasis;;;progression;drug resistance;metastasis;drug resistance;poor survival; pancreatic cancer;glioblastoma;sarcoma;breast cancer;sarcoma;prostate cancer;colorectal cancer;B cell lymphoma;ovarian cancer;colorectal cancer;liver cancer hsa-miR-181c-5p PTEN 1.58587920618301 1.57506918816933e-10 -0.452835975443078 0.00142504206837966 MirTarget;miRNATAP -0.127904121862523 2.20738602419631e-06 25695913 miR 181c promotes proliferation via suppressing PTEN expression in inflammatory breast cancer; In this study we showed that miR-181c as an oncogene promoted proliferation and it inhibited PTEN protein expression by targeting 3'-UTR of PTEN mRNA in IBC SUM149 cells; Thus targeting miR-181c and restoration of PTEN can be used in conjunction with other therapies to prevent progression of IBC progression breast cancer hsa-miR-181d-5p PTEN 1.52204912185579 9.2693319057748e-08 -0.452835975443078 0.00142504206837966 MirTarget -0.117066047918988 7.16131240625052e-07 27006767 Moreover hsa-miR-181d was upregulated to control expression a tumor suppressor gene PTEN to protect the cancer cell from apoptosis endometrial cancer hsa-miR-186-5p PTEN 1.47445398888668 3.0781726595413e-15 -0.452835975443078 0.00142504206837966 mirMAP;miRNATAP -0.221807059815679 3.24247402491438e-10 NA NA NA hsa-miR-188-5p PTEN 2.52825126596644 6.78099435999778e-14 -0.452835975443078 0.00142504206837966 MirTarget;PITA;miRNATAP -0.109812572617288 1.33705979957174e-07 NA NA NA hsa-miR-18a-5p PTEN 3.78535678765353 3.72446596213886e-26 -0.452835975443078 0.00142504206837966 miRNAWalker2_validate;miRTarBase -0.11423116163821 1.11808022110275e-09 24681249;27291152 However higher levels of the miR-17~92 cluster switched from PTEN to oncogenes including Ctnnb1 β-catenin via miR-18a which resulted in inhibition of tumor growth and metastasis;miR 18a promotes cell proliferation of esophageal squamous cell carcinoma cells by increasing cylin D1 via regulating PTEN PI3K AKT mTOR signaling axis metastasis; colon cancer;esophageal cancer hsa-miR-193a-3p PTEN 1.60460546928078 2.86169793322984e-07 -0.452835975443078 0.00142504206837966 PITA;miRanda -0.105979704931185 8.32668652705572e-07 26753960;23223432 Downregulation of microRNA 193 3p inhibits tumor proliferation migration and chemoresistance in human gastric cancer by regulating PTEN gene;Our study identifies miR-193a and PTEN as targets for AML1/ETO and provides evidence that links the epigenetic silencing of tumor suppressor genes miR-193a and PTEN to differentiation block of myeloid precursors drug resistance;differentiation gastric cancer;acute myeloid leukemia hsa-miR-19a-3p PTEN 3.42309334186656 3.02671914353412e-28 -0.452835975443078 0.00142504206837966 miRNAWalker2_validate;miRTarBase;MirTarget;miRNATAP -0.128463306420323 2.55472255726088e-10 25107371;27445062;26098000;24831732;21853360;24681249;27289489 The target of miR-19a was identified by western blot and whether its regulatory role depends on its target was improved by a rescue experiment with miR-19a mimic and PTEN expression plasmid; Meanwhile gain or loss of function of miR-19a demonstrated that miR-19a can promote cell growth of bladder cancer cells and the further mechanism studies indicated that its oncogenic role was dependent on targeting PTEN; The oncogenic role of miR19a in bladder cancer was dependent on targeting PTEN;The target genes of miR-19a such as ABCA1 and PTEN that had been suppressed by miR recovered their expression through CAP treatment;Moreover siRNA-mediated knockdown of PTEN a target of miR-19 also resulted in EMT migration and invasion of A549 and HCC827 cells suggesting that PTEN is involved in miR-19-induced EMT migration and invasion of lung cancer cells;Meanwhile BPA-induced upregulation of oncogenic miR-19a and miR-19b and the dysregulated expression of miR-19-related downstream proteins including PTEN p-AKT p-MDM2 p53 and proliferating cell nuclear antigen were reversed by curcumin;Regulation of miR 19 to breast cancer chemoresistance through targeting PTEN; Expression levels of miR-19 in MDR cells were inversely consistent with those of PTEN; Our findings demonstrate for the first time involvement of miR-19 in multidrug resistance through modulation of PTEN and suggest that miR-19 may be a potential target for preventing and reversing MDR in tumor cells;miR-19 in the context of the miR-17~92 cluster at medium levels promoted tumor metastasis through induction of Wnt/β-catenin-mediated epithelial-mesenchymal transition by targeting to the tumor-suppressor gene PTEN;Transfection of miR-19a and -19b mimics reversed the up-regulations of IGF2R and PTEN gene expression and abrogated the GSE induced anti-proliferative response ;;;;drug resistance;metastasis;drug resistance bladder cancer;breast cancer;lung cancer;breast cancer;breast cancer;colon cancer;lung cancer hsa-miR-19b-3p PTEN 2.49529833021187 1.57028265846699e-23 -0.452835975443078 0.00142504206837966 miRNAWalker2_validate;miRTarBase;MirTarget;miRNATAP -0.17043189646512 2.79115195694575e-11 26098000;24831732;21853360;24681249 Moreover siRNA-mediated knockdown of PTEN a target of miR-19 also resulted in EMT migration and invasion of A549 and HCC827 cells suggesting that PTEN is involved in miR-19-induced EMT migration and invasion of lung cancer cells;Meanwhile BPA-induced upregulation of oncogenic miR-19a and miR-19b and the dysregulated expression of miR-19-related downstream proteins including PTEN p-AKT p-MDM2 p53 and proliferating cell nuclear antigen were reversed by curcumin;Regulation of miR 19 to breast cancer chemoresistance through targeting PTEN; Expression levels of miR-19 in MDR cells were inversely consistent with those of PTEN; Our findings demonstrate for the first time involvement of miR-19 in multidrug resistance through modulation of PTEN and suggest that miR-19 may be a potential target for preventing and reversing MDR in tumor cells;miR-19 in the context of the miR-17~92 cluster at medium levels promoted tumor metastasis through induction of Wnt/β-catenin-mediated epithelial-mesenchymal transition by targeting to the tumor-suppressor gene PTEN ;;drug resistance;metastasis lung cancer;breast cancer;breast cancer;colon cancer hsa-miR-20a-5p PTEN 3.15577933619191 4.19753346442454e-25 -0.452835975443078 0.00142504206837966 miRNAWalker2_validate;miRTarBase;miRNATAP -0.12193642920165 5.77479259337628e-09 26031366 The expression of miR-20a and PTEN were detected in HCC cell lines and paired primary tissues by quantitative real-time polymerase chain reaction; MiR-20a levels were increased in HCC cell lines and tissues whereas PTEN was inversely correlated with it; PTEN was identified as a direct functional target of miR-20a for the induction of radioresistance drug resistance liver cancer hsa-miR-25-3p PTEN 1.36472605225697 4.83790725935681e-11 -0.452835975443078 0.00142504206837966 miRTarBase;MirTarget;miRNATAP -0.196462680546189 9.04767751306264e-10 NA NA NA hsa-miR-28-5p PTEN 0.230152919654905 0.0742909586754846 -0.452835975443078 0.00142504206837966 miRanda -0.112241090761127 0.0418761338534022 NA NA NA hsa-miR-301a-3p PTEN 2.81024345929638 2.29784847962242e-17 -0.452835975443078 0.00142504206837966 MirTarget;miRNATAP -0.123344981900917 2.76158051949627e-09 24315818;26846737 Upregulated microRNA 301a in breast cancer promotes tumor metastasis by targeting PTEN and activating Wnt/β catenin signaling; Furthermore miR-301a directly targeted and suppressed PTEN one negative regulator of the Wnt/β-catenin signaling cascade; These results demonstrate that miR-301a maintains constitutively activated Wnt/β-catenin signaling by directly targeting PTEN which promotes breast cancer invasion and metastasis;MicroRNA 301a promotes cell proliferation via PTEN targeting in Ewing's sarcoma cells; Our results demonstrated the novel mechanism controlling PTEN expression via miR-301a in ES cells metastasis; breast cancer;sarcoma hsa-miR-30b-5p PTEN 0.800822374912712 0.000133601914525413 -0.452835975443078 0.00142504206837966 mirMAP -0.15403930655305 2.2546089672267e-06 NA NA NA hsa-miR-30c-5p PTEN 0.778774633108 0.000285599212429136 -0.452835975443078 0.00142504206837966 mirMAP -0.150378554405459 2.29281374408959e-06 NA NA NA hsa-miR-30d-3p PTEN 0.977747550180601 4.3048212205381e-05 -0.452835975443078 0.00142504206837966 MirTarget;miRNATAP -0.119783791946268 2.73757307106354e-05 NA NA NA hsa-miR-30d-5p PTEN 0.675423997639582 0.00270618816039773 -0.452835975443078 0.00142504206837966 mirMAP -0.11072634618103 0.000287709940594657 NA NA NA hsa-miR-30e-5p PTEN 1.23904909539663 1.35561917122157e-09 -0.452835975443078 0.00142504206837966 mirMAP -0.160981204851498 1.03953643650469e-06 NA NA NA hsa-miR-32-5p PTEN 2.34056473219422 6.24134585974322e-20 -0.452835975443078 0.00142504206837966 MirTarget;miRNATAP -0.145568223802877 9.281864133748e-09 24123284;25647261;23617834 In this study we determined the levels of the correlation between and the clinical significance of the expression of miR-32 and phosphatase and tensin homologue PTEN a tumor suppressor targeted by miR-32 in CRC; The levels of miR-32 and PTEN gene expression in 35 colorectal carcinoma samples 35 corresponding cancer-adjacent tissue samples 27 colorectal adenoma samples and 16 normal tissue samples were quantified using real-time quantitative reverse transcriptase-polymerase chain reaction; The relationship between the miR-32 and PTEN protein expression and clinicopathological factors was analyzed; Significant upregulation of miR-32 expression and reduction of PTEN were identified in CRC tissues; An inverse relationship between miR-32 and PTEN protein expression was identified; MiR-32 and PTEN expression were inversely correlated and miR-32 may be associated with the development of CRC;MiR 32 induces cell proliferation migration and invasion in hepatocellular carcinoma by targeting PTEN; Besides miRNA-32 down-regulates PTEN through binding to 3'-UTR of PTEN mRNA from luciferase reporter assay and the expression level of miR-32 could affect the proliferation migration and invasion of liver cancer cell lines via PTEN/Akt signaling pathway; Down-expression of PTEN could significantly attenuate the inhibitory effects of knockdown miR-32 on the proliferation migration and invasion of liver cancer cells suggesting that miR-32 could be a potential target for HCC treatment;MicroRNA 32 miR 32 regulates phosphatase and tensin homologue PTEN expression and promotes growth migration and invasion in colorectal carcinoma cells; In this study we identified the potential effects of miR-32 on some important biological properties of CRC cells and clarified the regulation of PTEN by miR-32; The 3'-untranslated region 3'-UTR of PTEN combined with miR-32 was verified by dual-luciferase reporter assay; Gain-of-function and loss-of-function studies showed that overexpression of miR-32 promoted SW480 cell proliferation migration and invasion reduced apoptosis and resulted in downregulation of PTEN at a posttranscriptional level; However miR-32 knock-down inhibited these processes in HCT-116 cells and enhanced the expression of PTEN protein; In addition we further identified PTEN as the functional downstream target of miR-32 by directly targeting the 3'-UTR of PTEN; Our results demonstrated that miR-32 was involved in tumorigenesis of CRC at least in part by suppression of PTEN ;;tumorigenesis colorectal cancer;liver cancer;colorectal cancer hsa-miR-362-3p PTEN 2.0756816987665 3.89026064579331e-12 -0.452835975443078 0.00142504206837966 miRanda -0.115158238382692 5.24016404806603e-07 NA NA NA hsa-miR-363-3p PTEN 1.50575300026701 0.00020976164678918 -0.452835975443078 0.00142504206837966 MirTarget;miRNATAP -0.100220872472703 1.35166197069511e-09 NA NA NA hsa-miR-374a-5p PTEN 0.484615721953736 0.0042981729815149 -0.452835975443078 0.00142504206837966 MirTarget;mirMAP -0.154385867426133 0.000159063773613779 NA NA NA hsa-miR-374b-5p PTEN 0.0654362503857184 0.722673188879465 -0.452835975443078 0.00142504206837966 MirTarget;mirMAP;miRNATAP -0.119395270830768 0.00157844251632807 NA NA NA hsa-miR-421 PTEN 1.17791565395543 6.78526676976629e-06 -0.452835975443078 0.00142504206837966 miRanda -0.116149976062421 7.77520989006685e-06 NA NA NA hsa-miR-425-5p PTEN 3.07071373939774 4.02947460586085e-25 -0.452835975443078 0.00142504206837966 miRNATAP -0.139167264143658 8.36425767948797e-11 25154996 An increase in miR-425 depended upon IL-1β-induced NF-kappaB activation.Repression of PTEN by miR-425 promoted gastric cancer cell proliferation gastric cancer hsa-miR-454-3p PTEN 2.47234127820054 1.12878018736016e-21 -0.452835975443078 0.00142504206837966 MirTarget;miRNATAP -0.143498211514651 2.3895399060586e-08 26296312;27261580 MicroRNA 454 functions as an oncogene by regulating PTEN in uveal melanoma; Furthermore we identified PTEN as a direct target of miR-454; Our data revealed that ectopic expression of PTEN restored the effects of miR-454 on cell proliferation and invasion in uveal melanoma cells;MiR 454 promotes the progression of human non small cell lung cancer and directly targets PTEN; At last the potential regulatory function of miR-454 on PTEN expression was confirmed; Further PTEN was confirmed as a direct target of miR-454 by using Luciferase Reporter Assay ;progression melanoma;lung squamous cell cancer hsa-miR-484 PTEN 1.81844463411787 1.82951571230938e-15 -0.452835975443078 0.00142504206837966 miRNATAP -0.123242919063894 2.18866967044909e-05 NA NA NA hsa-miR-532-5p PTEN 1.55697650978597 1.57884735535196e-11 -0.452835975443078 0.00142504206837966 PITA;mirMAP;miRNATAP -0.144490491618683 5.83499130267459e-07 NA NA NA hsa-miR-590-5p PTEN 3.18300989862077 2.06813568597893e-26 -0.452835975443078 0.00142504206837966 mirMAP -0.121253713178443 3.04555241061884e-08 23803188 Targetscan predicted PDCD4 and PTEN as the potential target genes of miR-590-5p and miR-590-3p which was verified by luciferase reporter system and Western blotting liver cancer hsa-miR-7-1-3p PTEN 1.84950311431067 1.25300363397654e-13 -0.452835975443078 0.00142504206837966 mirMAP -0.133579523943701 4.98334583211167e-07 NA NA NA hsa-miR-92a-3p PTEN 2.06460102658973 1.44784291084757e-19 -0.452835975443078 0.00142504206837966 MirTarget;miRNATAP -0.175671660591697 6.62046894313789e-10 26432332;25515201;24137349;23546593;23133552;24026406 Downregulation of PTEN could mimic the same effects of miR-92a mimic in NSCLC cells and rescue the effects on NSCLC cells induced by miR-92a inhibitor; Taken together these findings suggested that miR-92a could promote growth metastasis and chemoresistance in NSCLC cells at least partially by targeting PTEN;MiR 92a Promotes Cell Metastasis of Colorectal Cancer Through PTEN Mediated PI3K/AKT Pathway; The expression of miR-92a PTEN and E-cadherin was analyzed by real-time PCR; In addition there was a negative correlation between levels of miR-92a and the PTEN gene p < 0.0001; The association of levels of miR-92a and PTEN with tumor cell migration in CRC was also confirmed in CRC cell models;MicroRNA miR-92 is overexpressed in a number of tumors and has been proven to negatively regulate a number of tumor suppressor genes including phosphatase and tensin homologue PTEN; PTEN protein expression was decreased in the SiHa cells that were transfected with the miR-92 mimic; The data indicated that miR-92 may increase the migration and invasion of SiHa cells partially through the downregulation of PTEN protein expression;Expression and significance of PTEN and miR 92 in hepatocellular carcinoma; Immunohistochemistry streptavidin-peroxidase SP and quantitative reverse transcriptase-polymerase chain reaction qRT‑PCR were used to detect the expression of PTEN and miR-92 in 15 cases of HCC and the corresponding paracancerous tissues; The correlation between PTEN and miR-92 was analyzed; Additionally the mRNA levels of PTEN and miR-92 showed a significantly negative correlation with each other r=-0.858 P<0.05; In conclusion PTEN and miR-92 have different roles in the development of HCC; The combined detection of PTEN and miR-92 may provide critical clinical evidence for the early diagnosis and prognosis of HCC;PTEN mRNA correlated inversely with miR-92a and members of the miR-17 and miR-130/301 families;The expression levels of miR-92a and phosphatase and tensin homologue PTEN were detected by qRT-PCR and western blot; In addition the regulation of PTEN by miR-92a was evaluated by qRT-PCR western blot and luciferase reporter assays; There was an inverse correlation between the levels of miR-92a and PTEN in CRC tissues; The overexpression of miR-92a in CRC cells decreased PTEN expression at the translational level and decreased PTEN-driven luciferase-reporter activity; Our results demonstrated that miR-92a induced EMT and regulated cell growth migration and invasion in the SW480 cells at least partially via suppression of PTEN expression metastasis;drug resistance;metastasis;cell migration;;worse prognosis;; lung squamous cell cancer;colorectal cancer;cervical and endocervical cancer;liver cancer;sarcoma;colorectal cancer hsa-miR-92b-3p PTEN 1.20409245530001 3.41055816361655e-06 -0.452835975443078 0.00142504206837966 MirTarget;miRNATAP -0.114974293673639 1.10439131275336e-05 24099768;26878388;24137349;23546593 MiR 92b regulates the cell growth cisplatin chemosensitivity of A549 non small cell lung cancer cell line and target PTEN; Furthermore we found miR-92b could directly target PTEN a unique tumor suppressor gene which was downregulated in lung cancer tissues compared to the matched adjacent normal tissues;We revealed that patients exhibiting an upregulation of hsa-miR-92b and patients with deletions of PTEN did not tend to overlap and hsa-miR-92b and PTEN coordinately regulated the pathway of 'cell cycle' and so on;MicroRNA miR-92 is overexpressed in a number of tumors and has been proven to negatively regulate a number of tumor suppressor genes including phosphatase and tensin homologue PTEN; PTEN protein expression was decreased in the SiHa cells that were transfected with the miR-92 mimic; The data indicated that miR-92 may increase the migration and invasion of SiHa cells partially through the downregulation of PTEN protein expression;Expression and significance of PTEN and miR 92 in hepatocellular carcinoma; Immunohistochemistry streptavidin-peroxidase SP and quantitative reverse transcriptase-polymerase chain reaction qRT‑PCR were used to detect the expression of PTEN and miR-92 in 15 cases of HCC and the corresponding paracancerous tissues; The correlation between PTEN and miR-92 was analyzed; Additionally the mRNA levels of PTEN and miR-92 showed a significantly negative correlation with each other r=-0.858 P<0.05; In conclusion PTEN and miR-92 have different roles in the development of HCC; The combined detection of PTEN and miR-92 may provide critical clinical evidence for the early diagnosis and prognosis of HCC ;;;worse prognosis lung squamous cell cancer;breast cancer;cervical and endocervical cancer;liver cancer hsa-miR-93-5p PTEN 3.03961860136032 1.11672209617395e-24 -0.452835975443078 0.00142504206837966 miRNAWalker2_validate;miRTarBase;miRNATAP -0.134735169835666 3.72873311860152e-10 25633810;26243299;22465665;26087719 MicroRNA 93 activates c Met/PI3K/Akt pathway activity in hepatocellular carcinoma by directly inhibiting PTEN and CDKN1A; We confirmed that miR-93 directly bound with the 3' untranslated regions of the tumor-suppressor genes PTEN and CDKN1A respectivelyand inhibited their expression; We concluded that miR-93 stimulated cell proliferation migration and invasion through the oncogenic c-Met/PI3K/Akt pathway and also inhibited apoptosis by directly inhibiting PTEN and CDKN1A expression in human HCC;microRNA 93 promotes cell proliferation via targeting of PTEN in Osteosarcoma cells; An miRNA miR-93 was significantly up-regulated whereas phosphatase and tensin homologue PTEN expression was significantly down-regulated in all tested OS cells when compared with hMSCs; Ectopic expression of miR-93 decreased PTEN protein levels; Taking these observations together miR-93 can be seen to play a critical role in carcinogenesis through suppression of PTEN and may serve as a therapeutic target for the treatment of OS;Furthermore we found that miR-93 can directly target PTEN and participates in the regulation of the AKT signaling pathway; MiR-93 inversely correlates with PTEN expression in CDDP-resistant and sensitive human ovarian cancer tissues;Furthermore our study found berberine could inhibit miR-93 expression and function in ovarian cancer as shown by an increase of its target PTEN an important tumor suppressor in ovarian cancer; More importantly A2780 cells that were treated with PTEN siRNA had a survival pattern that is similar to cells with miR-93 overexpression ;tumorigenesis;;poor survival liver cancer;sarcoma;ovarian cancer;ovarian cancer