| Num |
microRNA |
Gene |
miRNA log2FC |
miRNA pvalue |
Gene log2FC |
Gene pvalue |
Interaction |
Correlation beta |
Correlation P-value |
PMID |
Reported in cancer studies |
| 1 |
hsa-miR-103a-3p |
PTEN |
1.44 |
0 |
-0.45 |
0.00143 |
miRNAWalker2 validate; miRTarBase |
-0.18 |
0 |
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 |
| 2 |
hsa-miR-106a-5p |
PTEN |
2.49 |
0 |
-0.45 |
0.00143 |
miRNATAP |
-0.12 |
0 |
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 |
| 3 |
hsa-miR-106b-5p |
PTEN |
2.47 |
0 |
-0.45 |
0.00143 |
miRNAWalker2 validate; miRTarBase; miRNATAP |
-0.17 |
0 |
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 |
| 4 |
hsa-miR-107 |
PTEN |
1.31 |
0 |
-0.45 |
0.00143 |
miRNAWalker2 validate; PITA; miRanda |
-0.13 |
0.00031 |
|
NA |
| 5 |
hsa-miR-130a-3p |
PTEN |
2.02 |
0 |
-0.45 |
0.00143 |
MirTarget; miRNATAP |
-0.11 |
0 |
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 |
| 6 |
hsa-miR-130b-3p |
PTEN |
3.54 |
0 |
-0.45 |
0.00143 |
MirTarget; miRNATAP |
-0.12 |
0 |
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 |
| 7 |
hsa-miR-148a-3p |
PTEN |
1.27 |
0 |
-0.45 |
0.00143 |
MirTarget; miRNATAP |
-0.1 |
5.0E-5 |
22496917 |
Introduction of anti-miR-148a increased PTEN protein and mRNA expression suggesting that PTEN was targeted by miR-148a |
| 8 |
hsa-miR-148b-3p |
PTEN |
1.98 |
0 |
-0.45 |
0.00143 |
MirTarget; miRNATAP |
-0.17 |
0 |
|
NA |
| 9 |
hsa-miR-15b-3p |
PTEN |
2.34 |
0 |
-0.45 |
0.00143 |
mirMAP |
-0.11 |
1.0E-5 |
|
NA |
| 10 |
hsa-miR-16-2-3p |
PTEN |
2.32 |
0 |
-0.45 |
0.00143 |
mirMAP |
-0.1 |
8.0E-5 |
|
NA |
| 11 |
hsa-miR-17-5p |
PTEN |
3.27 |
0 |
-0.45 |
0.00143 |
miRNAWalker2 validate; miRTarBase; TargetScan; miRNATAP |
-0.13 |
0 |
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 |
| 12 |
hsa-miR-181c-5p |
PTEN |
1.59 |
0 |
-0.45 |
0.00143 |
MirTarget; miRNATAP |
-0.13 |
0 |
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 |
| 13 |
hsa-miR-181d-5p |
PTEN |
1.52 |
0 |
-0.45 |
0.00143 |
MirTarget |
-0.12 |
0 |
27006767 |
Moreover hsa-miR-181d was upregulated to control expression a tumor suppressor gene PTEN to protect the cancer cell from apoptosis |
| 14 |
hsa-miR-186-5p |
PTEN |
1.47 |
0 |
-0.45 |
0.00143 |
mirMAP; miRNATAP |
-0.22 |
0 |
|
NA |
| 15 |
hsa-miR-188-5p |
PTEN |
2.53 |
0 |
-0.45 |
0.00143 |
MirTarget; PITA; miRNATAP |
-0.11 |
0 |
|
NA |
| 16 |
hsa-miR-18a-5p |
PTEN |
3.79 |
0 |
-0.45 |
0.00143 |
miRNAWalker2 validate; miRTarBase |
-0.11 |
0 |
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 |
| 17 |
hsa-miR-193a-3p |
PTEN |
1.6 |
0 |
-0.45 |
0.00143 |
PITA; miRanda |
-0.11 |
0 |
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 |
| 18 |
hsa-miR-19a-3p |
PTEN |
3.42 |
0 |
-0.45 |
0.00143 |
miRNAWalker2 validate; miRTarBase; MirTarget; miRNATAP |
-0.13 |
0 |
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 |
| 19 |
hsa-miR-19b-3p |
PTEN |
2.5 |
0 |
-0.45 |
0.00143 |
miRNAWalker2 validate; miRTarBase; MirTarget; miRNATAP |
-0.17 |
0 |
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 |
| 20 |
hsa-miR-20a-5p |
PTEN |
3.16 |
0 |
-0.45 |
0.00143 |
miRNAWalker2 validate; miRTarBase; miRNATAP |
-0.12 |
0 |
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 |
| 21 |
hsa-miR-25-3p |
PTEN |
1.36 |
0 |
-0.45 |
0.00143 |
miRTarBase; MirTarget; miRNATAP |
-0.2 |
0 |
|
NA |
| 22 |
hsa-miR-28-5p |
PTEN |
0.23 |
0.07429 |
-0.45 |
0.00143 |
miRanda |
-0.11 |
0.04188 |
|
NA |
| 23 |
hsa-miR-301a-3p |
PTEN |
2.81 |
0 |
-0.45 |
0.00143 |
MirTarget; miRNATAP |
-0.12 |
0 |
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 |
| 24 |
hsa-miR-30b-5p |
PTEN |
0.8 |
0.00013 |
-0.45 |
0.00143 |
mirMAP |
-0.15 |
0 |
|
NA |
| 25 |
hsa-miR-30c-5p |
PTEN |
0.78 |
0.00029 |
-0.45 |
0.00143 |
mirMAP |
-0.15 |
0 |
|
NA |
| 26 |
hsa-miR-30d-3p |
PTEN |
0.98 |
4.0E-5 |
-0.45 |
0.00143 |
MirTarget; miRNATAP |
-0.12 |
3.0E-5 |
|
NA |
| 27 |
hsa-miR-30d-5p |
PTEN |
0.68 |
0.00271 |
-0.45 |
0.00143 |
mirMAP |
-0.11 |
0.00029 |
|
NA |
| 28 |
hsa-miR-30e-5p |
PTEN |
1.24 |
0 |
-0.45 |
0.00143 |
mirMAP |
-0.16 |
0 |
|
NA |
| 29 |
hsa-miR-32-5p |
PTEN |
2.34 |
0 |
-0.45 |
0.00143 |
MirTarget; miRNATAP |
-0.15 |
0 |
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 |
| 30 |
hsa-miR-362-3p |
PTEN |
2.08 |
0 |
-0.45 |
0.00143 |
miRanda |
-0.12 |
0 |
|
NA |
| 31 |
hsa-miR-363-3p |
PTEN |
1.51 |
0.00021 |
-0.45 |
0.00143 |
MirTarget; miRNATAP |
-0.1 |
0 |
|
NA |
| 32 |
hsa-miR-374a-5p |
PTEN |
0.48 |
0.0043 |
-0.45 |
0.00143 |
MirTarget; mirMAP |
-0.15 |
0.00016 |
|
NA |
| 33 |
hsa-miR-374b-5p |
PTEN |
0.07 |
0.72267 |
-0.45 |
0.00143 |
MirTarget; mirMAP; miRNATAP |
-0.12 |
0.00158 |
|
NA |
| 34 |
hsa-miR-421 |
PTEN |
1.18 |
1.0E-5 |
-0.45 |
0.00143 |
miRanda |
-0.12 |
1.0E-5 |
|
NA |
| 35 |
hsa-miR-425-5p |
PTEN |
3.07 |
0 |
-0.45 |
0.00143 |
miRNATAP |
-0.14 |
0 |
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 |
| 36 |
hsa-miR-454-3p |
PTEN |
2.47 |
0 |
-0.45 |
0.00143 |
MirTarget; miRNATAP |
-0.14 |
0 |
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 |
| 37 |
hsa-miR-484 |
PTEN |
1.82 |
0 |
-0.45 |
0.00143 |
miRNATAP |
-0.12 |
2.0E-5 |
|
NA |
| 38 |
hsa-miR-532-5p |
PTEN |
1.56 |
0 |
-0.45 |
0.00143 |
PITA; mirMAP; miRNATAP |
-0.14 |
0 |
|
NA |
| 39 |
hsa-miR-590-5p |
PTEN |
3.18 |
0 |
-0.45 |
0.00143 |
mirMAP |
-0.12 |
0 |
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 |
| 40 |
hsa-miR-7-1-3p |
PTEN |
1.85 |
0 |
-0.45 |
0.00143 |
mirMAP |
-0.13 |
0 |
|
NA |
| 41 |
hsa-miR-92a-3p |
PTEN |
2.06 |
0 |
-0.45 |
0.00143 |
MirTarget; miRNATAP |
-0.18 |
0 |
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 |
| 42 |
hsa-miR-92b-3p |
PTEN |
1.2 |
0 |
-0.45 |
0.00143 |
MirTarget; miRNATAP |
-0.11 |
1.0E-5 |
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 |
| 43 |
hsa-miR-93-5p |
PTEN |
3.04 |
0 |
-0.45 |
0.00143 |
miRNAWalker2 validate; miRTarBase; miRNATAP |
-0.13 |
0 |
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 |
