Explanation
This regulatory network was inferred from the input dataset. The miRNAs and mRNAs are
presented as round and rectangle nodes respectively. The numerical value popped up upon mouse over the gene node is the log2 transformed fold-change of the gene expression between the two groups. All of the nodes are clickable, and the detailed information of the miRNAs/mRNAs and related cancer pathway will be displayed in another window. The edges between nodes are supported by both interactions (predicted or experimentally verified) and correlations learnt from cancer dataset. The numerical value popped up upon mouse over the edge is the correlation beat value (effect size) between the two nodes. The experimental evidences of the edges reported in previous cancer studies are highlighted by red/orange color. All of these information can be accessed by the "mouse-over" action. This network shows a full map of the miRNA-mRNA regulation of the input gene list(s), and the hub miRNAs (with the high network degree/betweenness centrality) would be the potential cancer drivers or tumor suppressors. The full result table can be accessed in the "Regulations" tab.
"miRNACancerMAP" is also a network visualization tool for users to draw their regulatory network by personal customization. Users can set the complexity of the network by limiting the number of nodes or edges. And the color of the nodes can be defined by different categories of the mRNAs and miRNAs, such as Gene-Ontology, pathway, and expression status. Users can also select to use network degree or network betweenness centrality to define the node size. And edges can be black or colored by the correlation. Purple edge means negative correlation (mostly found between miRNA and mRNA), and blue edge means positive correlation (found in PPI or miRNA-miRNA sponge effect). We can also add the protein-protein interactions (PPI) into the network. This result will show the cluster of genes regulated by some specific miRNAs. Additionally, miRNA-miRNA edges can be added by the "miRNA sponge" button, presenting some clusters of miRNAs that have the interactions via sponge effect.
miRNA-gene regulations
| 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-30d-5p | CASP3 | -0.92 | 4.0E-5 | 0.75 | 0 | miRNAWalker2 validate; miRTarBase; miRNATAP | -0.17 | 0 | NA | |
| 2 | hsa-miR-106a-5p | CCND1 | 1.39 | 6.0E-5 | -0.3 | 0.2554 | MirTarget; miRNATAP | -0.25 | 0 | NA | |
| 3 | hsa-miR-106b-5p | CCND1 | 1.47 | 0 | -0.3 | 0.2554 | miRNAWalker2 validate; miRTarBase; MirTarget; miRNATAP | -0.26 | 1.0E-5 | NA | |
| 4 | hsa-miR-15a-5p | CCND1 | 1.63 | 0 | -0.3 | 0.2554 | miRNAWalker2 validate; miRTarBase; MirTarget; miRNATAP | -0.2 | 0.00193 | 22922827 | CCND1 has been found to be a target of miR-15a and miR-16-1 through analysis of complementary sequences between microRNAs and CCND1 mRNA; Moreover the transcription of CCND1 is suppressed by miR-15a and miR-16-1 via direct binding to the CCND1 3'-untranslated region 3'-UTR |
| 5 | hsa-miR-15b-5p | CCND1 | -1.26 | 0 | -0.3 | 0.2554 | miRNAWalker2 validate; miRTarBase; MirTarget; miRNATAP | -0.3 | 0 | NA | |
| 6 | hsa-miR-16-1-3p | CCND1 | 1.5 | 0 | -0.3 | 0.2554 | miRNAWalker2 validate; miRTarBase | -0.25 | 3.0E-5 | 22922827; 18483394 | CCND1 has been found to be a target of miR-15a and miR-16-1 through analysis of complementary sequences between microRNAs and CCND1 mRNA; Moreover the transcription of CCND1 is suppressed by miR-15a and miR-16-1 via direct binding to the CCND1 3'-untranslated region 3'-UTR;Truncation in CCND1 mRNA alters miR 16 1 regulation in mantle cell lymphoma; Furthermore we demonstrated that this truncation alters miR-16-1 binding sites and through the use of reporter constructs we were able to show that miR-16-1 regulates CCND1 mRNA expression; This study introduces the role of miR-16-1 in the regulation of CCND1 in MCL |
| 7 | hsa-miR-16-5p | CCND1 | 0.75 | 0 | -0.3 | 0.2554 | miRNAWalker2 validate; miRTarBase; MirTarget; miRNATAP | -0.37 | 0 | 23991964; 22922827; 18483394 | At the molecular level our results further revealed that cyclin D1 expression was negatively regulated by miR-16;CCND1 has been found to be a target of miR-15a and miR-16-1 through analysis of complementary sequences between microRNAs and CCND1 mRNA; Moreover the transcription of CCND1 is suppressed by miR-15a and miR-16-1 via direct binding to the CCND1 3'-untranslated region 3'-UTR;Truncation in CCND1 mRNA alters miR 16 1 regulation in mantle cell lymphoma; Furthermore we demonstrated that this truncation alters miR-16-1 binding sites and through the use of reporter constructs we were able to show that miR-16-1 regulates CCND1 mRNA expression; This study introduces the role of miR-16-1 in the regulation of CCND1 in MCL |
| 8 | hsa-miR-17-5p | CCND1 | 2.07 | 0 | -0.3 | 0.2554 | miRNAWalker2 validate; MirTarget; TargetScan; miRNATAP | -0.31 | 0 | 26431674 | Bioinformatics Prediction and In Vitro Analysis Revealed That miR 17 Targets Cyclin D1 mRNA in Triple Negative Breast Cancer Cells; In this study using bioinformatic analyses miR-17 was selected as it targets the 3'UTR of CCND1 gene with the highest score; After lentiviral transduction of miR-17 to the target cells gene expression analysis showed decreased expression of CCND1 gene |
| 9 | hsa-miR-193a-3p | CCND1 | 0.55 | 0.0319 | -0.3 | 0.2554 | MirTarget; PITA; miRanda | -0.19 | 0.00016 | NA | |
| 10 | hsa-miR-193b-3p | CCND1 | 1.1 | 0.00082 | -0.3 | 0.2554 | miRNAWalker2 validate; miRTarBase; MirTarget | -0.15 | 4.0E-5 | 27071318; 20655737; 20304954; 21893020; 26129688 | MicroRNA 193b inhibits the proliferation migration and invasion of gastric cancer cells via targeting cyclin D1; Further mechanism study indicated that CCND1 was a direct target of miR-193b in GC;CCND1 and ETS1 were revealed to be regulated by miR-193b directly;MicroRNA 193b represses cell proliferation and regulates cyclin D1 in melanoma; Overexpression of miR-193b in Malme-3M cells down-regulated CCND1 mRNA and protein by > or = 50%; A luciferase reporter assay confirmed that miR-193b directly regulates CCND1 by binding to the 3'untranslated region of CCND1 mRNA; These studies indicate that miR-193b represses cell proliferation and regulates CCND1 expression and suggest that dysregulation of miR-193b may play an important role in melanoma development;In a previous study we reported that miR-193b represses cell proliferation and regulates cyclin D1 in melanoma cells suggesting that miR-193b could act as a tumor suppressor;Epigenetically altered miR 193b targets cyclin D1 in prostate cancer; It has been suggested that miR-193b targets cyclin D1 in several malignancies; Here our aim was to determine if miR-193b targets cyclin D1 in prostate cancer; Furthermore the PC cell lines 22Rv1 and VCaP which express low levels of miR-193b and high levels of CCND1 showed significant growth retardation when treated with a CDK4/6 inhibitor; In contrast the inhibitor had no effect on the growth of PC-3 and DU145 cells with high miR-193b and low CCND1 expression; Taken together our data demonstrate that miR-193b targets cyclin D1 in prostate cancer |
| 11 | hsa-miR-19a-3p | CCND1 | 2.12 | 0 | -0.3 | 0.2554 | miRNAWalker2 validate; miRTarBase; miRNATAP | -0.22 | 0 | 25985117 | Moreover miR-19a might play inhibitory roles in HCC malignancy via regulating Cyclin D1 expression |
| 12 | hsa-miR-19b-1-5p | CCND1 | 1.71 | 0 | -0.3 | 0.2554 | miRNAWalker2 validate; miRTarBase | -0.3 | 0 | NA | |
| 13 | hsa-miR-20a-5p | CCND1 | 2.65 | 0 | -0.3 | 0.2554 | miRNAWalker2 validate; miRTarBase; MirTarget; miRNATAP | -0.24 | 0 | NA | |
| 14 | hsa-miR-20b-5p | CCND1 | 1.36 | 0.00261 | -0.3 | 0.2554 | MirTarget; miRNATAP | -0.18 | 0 | NA | |
| 15 | hsa-miR-365a-3p | CCND1 | 0.01 | 0.9536 | -0.3 | 0.2554 | miRNAWalker2 validate; miRTarBase | -0.19 | 0.00023 | NA | |
| 16 | hsa-miR-374b-5p | CCND1 | 0.47 | 0.01092 | -0.3 | 0.2554 | miRNAWalker2 validate; MirTarget | -0.26 | 0.00012 | NA | |
| 17 | hsa-miR-93-5p | CCND1 | 1.51 | 0 | -0.3 | 0.2554 | miRNAWalker2 validate; MirTarget; miRNATAP | -0.32 | 0 | NA | |
| 18 | hsa-miR-106b-5p | CCND2 | 1.47 | 0 | -1.64 | 0 | miRNAWalker2 validate; miRTarBase; miRNATAP | -0.38 | 0 | NA | |
| 19 | hsa-miR-141-3p | CCND2 | 3.37 | 0 | -1.64 | 0 | MirTarget; TargetScan | -0.24 | 0 | NA | |
| 20 | hsa-miR-15a-5p | CCND2 | 1.63 | 0 | -1.64 | 0 | miRNAWalker2 validate; miRTarBase; miRNATAP | -0.16 | 0.00712 | NA | |
| 21 | hsa-miR-16-5p | CCND2 | 0.75 | 0 | -1.64 | 0 | miRNAWalker2 validate; miRNATAP | -0.14 | 0.04485 | NA | |
| 22 | hsa-miR-17-5p | CCND2 | 2.07 | 0 | -1.64 | 0 | miRNAWalker2 validate; miRTarBase; TargetScan; miRNATAP | -0.37 | 0 | NA | |
| 23 | hsa-miR-182-5p | CCND2 | 3.22 | 0 | -1.64 | 0 | miRNAWalker2 validate; miRTarBase; miRNATAP | -0.37 | 0 | NA | |
| 24 | hsa-miR-185-5p | CCND2 | 1.14 | 0 | -1.64 | 0 | MirTarget; miRNATAP | -0.24 | 0.00048 | NA | |
| 25 | hsa-miR-186-5p | CCND2 | 0.85 | 0 | -1.64 | 0 | mirMAP; miRNATAP | -0.36 | 1.0E-5 | NA | |
| 26 | hsa-miR-19a-3p | CCND2 | 2.12 | 0 | -1.64 | 0 | MirTarget; miRNATAP | -0.17 | 1.0E-5 | NA | |
| 27 | hsa-miR-19b-3p | CCND2 | 2.11 | 0 | -1.64 | 0 | miRNAWalker2 validate; MirTarget; miRNATAP | -0.19 | 1.0E-5 | NA | |
| 28 | hsa-miR-20a-5p | CCND2 | 2.65 | 0 | -1.64 | 0 | miRNAWalker2 validate; miRTarBase; miRNATAP | -0.28 | 0 | NA | |
| 29 | hsa-miR-320b | CCND2 | 0.23 | 0.37882 | -1.64 | 0 | mirMAP; miRNATAP | -0.12 | 0.00373 | NA | |
| 30 | hsa-miR-450b-5p | CCND2 | 1.69 | 0 | -1.64 | 0 | MirTarget; PITA; miRNATAP | -0.15 | 9.0E-5 | NA | |
| 31 | hsa-miR-501-5p | CCND2 | 0.41 | 0.10435 | -1.64 | 0 | PITA; mirMAP; miRNATAP | -0.14 | 0.00086 | NA | |
| 32 | hsa-miR-590-3p | CCND2 | 0.84 | 0.00129 | -1.64 | 0 | miRanda; mirMAP | -0.13 | 0.00821 | NA | |
| 33 | hsa-miR-96-5p | CCND2 | 3.04 | 0 | -1.64 | 0 | TargetScan; miRNATAP | -0.36 | 0 | NA | |
| 34 | hsa-miR-421 | CCND3 | 0.17 | 0.53528 | -0.86 | 1.0E-5 | PITA; miRanda | -0.12 | 0.00073 | NA | |
| 35 | hsa-miR-195-5p | CCNE1 | -1.02 | 5.0E-5 | 3 | 0 | miRNAWalker2 validate; MirTarget; miRNATAP | -0.52 | 0 | 24402230 | Furthermore through qPCR and western blot assays we showed that overexpression of miR-195-5p reduced CCNE1 mRNA and protein levels respectively |
| 36 | hsa-miR-26a-5p | CCNE1 | -0.13 | 0.44003 | 3 | 0 | miRNAWalker2 validate; miRTarBase; miRNATAP | -0.7 | 0 | 22094936 | Cell cycle regulation and CCNE1 and CDC2 were the only significant overlapping pathway and genes differentially expressed between tumors with high and low levels of miR-26a and EZH2 respectively; Low mRNA levels of EZH2 CCNE1 and CDC2 and high levels of miR-26a are associated with favorable outcome on tamoxifen |
| 37 | hsa-miR-497-5p | CCNE1 | -0.05 | 0.78621 | 3 | 0 | MirTarget; miRNATAP | -0.5 | 0 | 25909221; 24112607; 24909281 | The effect of simultaneous overexpression of miR-497 and miR-34a on the inhibition of cell proliferation colony formation and tumor growth and the downregulation of cyclin E1 was stronger than the effect of each miRNA alone; The synergistic actions of miR-497 and miR-34a partly correlated with cyclin E1 levels; These results indicate cyclin E1 is downregulated by both miR-497 and miR-34a which synergistically retard the growth of human lung cancer cells;Western blot assays confirmed that overexpression of miR-497 reduced cyclin E1 protein levels; Inhibited cellular growth suppressed cellular migration and invasion and G1 cell cycle arrest were observed upon overexpression of miR-497 in cells possibly by targeting cyclin E1;miR 497 suppresses proliferation of human cervical carcinoma HeLa cells by targeting cyclin E1; Furthermore the target effect of miR-497 on the CCNE1 was identified by dual-luciferase reporter assay system qRT-PCR and Western blotting; Over-expressed miR-497 in HeLa cells could suppress cell proliferation by targeting CCNE1 |
| 38 | hsa-miR-26a-5p | CCNE2 | -0.13 | 0.44003 | 2.15 | 0 | miRNAWalker2 validate; miRTarBase; miRNATAP | -0.51 | 0 | 24116110; 21901171 | The loss of miR 26a mediated post transcriptional regulation of cyclin E2 in pancreatic cancer cell proliferation and decreased patient survival; The in vitro and in vivo assays showed that overexpression of miR-26a resulted in cell cycle arrest inhibited cell proliferation and decreased tumor growth which was associated with cyclin E2 downregulation;We also show that enforced expression of miR-26a in AML cells is able to inhibit cell cycle progression by downregulating cyclin E2 expression |
| 39 | hsa-miR-30b-5p | CCNE2 | 0.36 | 0.13803 | 2.15 | 0 | miRNAWalker2 validate; miRTarBase | -0.2 | 0.0005 | 22384020 | A luciferase-based reporter assay demonstrated that miR-30b post-transcriptionally reduced 27% p = 0.005 of the gene expression by interacting with two binding sites in the 3'-UTR of CCNE2; The upregulation of miR-30b by trastuzumab may play a biological role in trastuzumab-induced cell growth inhibition by targeting CCNE2 |
| 40 | hsa-miR-34a-5p | CCNE2 | 1.41 | 0 | 2.15 | 0 | miRNAWalker2 validate; miRTarBase; miRNATAP | -0.2 | 0.00337 | NA | |
| 41 | hsa-miR-34c-5p | CCNE2 | -1 | 0.07244 | 2.15 | 0 | miRNAWalker2 validate; miRTarBase; PITA; miRanda; miRNATAP | -0.11 | 4.0E-5 | NA | |
| 42 | hsa-miR-23a-3p | CCNG1 | 0.11 | 0.39309 | -0.38 | 0.02147 | MirTarget; miRNATAP | -0.18 | 0.00203 | NA | |
| 43 | hsa-miR-27a-3p | CCNG1 | 0.43 | 0.00737 | -0.38 | 0.02147 | MirTarget; miRNATAP | -0.25 | 0 | NA | |
| 44 | hsa-miR-27b-3p | CCNG1 | 0.24 | 0.12264 | -0.38 | 0.02147 | MirTarget; miRNATAP | -0.17 | 0.00064 | 26623719 | Moreover miR-27b directly targets the 3' untranslated regions 3'-UTRs of CCNG1 a well-known negative regulator of P53 stability; Interestingly miR-27b up-regulation leads to increased miR-508-5p expression and this phenomenon is mediated by CCNG1 and P53 |
| 45 | hsa-miR-96-5p | CCNG1 | 3.04 | 0 | -0.38 | 0.02147 | MirTarget; TargetScan | -0.13 | 1.0E-5 | NA | |
| 46 | hsa-miR-664a-3p | CCNG2 | 0.44 | 0.02142 | 0.22 | 0.10548 | MirTarget; mirMAP | -0.16 | 0 | NA | |
| 47 | hsa-miR-145-5p | CDK4 | -1.35 | 0 | 0.74 | 1.0E-5 | miRNAWalker2 validate; miRTarBase | -0.15 | 0 | 21092188 | Furthermore we found that CDK4 was regulated by miR-145 in cell cycle control |
| 48 | hsa-miR-195-5p | CDK4 | -1.02 | 5.0E-5 | 0.74 | 1.0E-5 | miRNAWalker2 validate; miRTarBase | -0.11 | 0.00037 | NA | |
| 49 | hsa-miR-24-3p | CDK4 | -0.04 | 0.78587 | 0.74 | 1.0E-5 | miRNAWalker2 validate; miRTarBase | -0.12 | 0.04666 | NA | |
| 50 | hsa-miR-141-3p | CDK6 | 3.37 | 0 | -0.63 | 0.01747 | TargetScan; miRNATAP | -0.16 | 6.0E-5 | NA | |
| 51 | hsa-miR-21-5p | CDK6 | 4.38 | 0 | -0.63 | 0.01747 | miRNAWalker2 validate; mirMAP | -0.15 | 0.00158 | NA | |
| 52 | hsa-miR-29b-3p | CDK6 | 3.11 | 0 | -0.63 | 0.01747 | miRNAWalker2 validate; miRTarBase; miRNATAP | -0.18 | 4.0E-5 | 23591808; 23245396; 25472644; 26180082; 27230400; 20086245 | Here we have identified the oncogene cyclin-dependent protein kinase 6 CDK6 as a direct target of miR-29b in lung cancer;The IFN-γ-induced G1-arrest of melanoma cells involves down-regulation of CDK6 which we proved to be a direct target of miR-29 in these cells;Moreover miR-29b inhibited the expression of MCL1 and CDK6;Knockdown of NTSR1 increased the expression of miR-29b-1 and miR-129-3p which were responsible for the decreased CDK6 expression;MiR 29b suppresses the proliferation and migration of osteosarcoma cells by targeting CDK6; In this study we investigated the role of miR-29b as a novel regulator of CDK6 using bioinformatics methods; We demonstrated that CDK6 can be downregulated by miR-29b via binding to the 3'-UTR region in osteosarcoma cells; Furthermore we identified an inverse correlation between miR-29b and CDK6 protein levels in osteosarcoma tissues; The results revealed that miR-29b acts as a tumor suppressor of osteosarcoma by targeting CDK6 in the proliferation and migration processes;microRNA expression profile and identification of miR 29 as a prognostic marker and pathogenetic factor by targeting CDK6 in mantle cell lymphoma; Furthermore we demonstrate miR-29 inhibition of CDK6 protein and mRNA levels by direct binding to 3'-untranslated region; Inverse correlation between miR-29 and CDK6 was observed in MCL |
| 53 | hsa-miR-34a-5p | CDK6 | 1.41 | 0 | -0.63 | 0.01747 | miRNAWalker2 validate; miRTarBase; miRNATAP | -0.24 | 3.0E-5 | 26104764; 21702042 | The expression of microRNA 34a is inversely correlated with c MET and CDK6 and has a prognostic significance in lung adenocarcinoma patients; We found significant inverse correlations between miR-34a and c-MET R = -0.316 P = 0.028 and CDK6 expression R = -0.4582 P = 0.004;Molecular analyses identified Cdk6 and sirtuin SIRT-1 as being targeted by miR-34a in MI-TCC cells however inhibition of Cdk6 and SIRT-1 was not as effective as pre-miR-34a in mediating chemosensitization |
| 54 | hsa-miR-429 | CDK6 | 2.38 | 0 | -0.63 | 0.01747 | mirMAP; miRNATAP | -0.15 | 0.00018 | NA | |
| 55 | hsa-miR-106b-5p | CDKN1A | 1.47 | 0 | -0.99 | 0 | miRNAWalker2 validate; miRTarBase; MirTarget; miRNATAP | -0.23 | 0 | NA | |
| 56 | hsa-miR-17-5p | CDKN1A | 2.07 | 0 | -0.99 | 0 | miRNAWalker2 validate; miRTarBase; MirTarget; TargetScan; miRNATAP | -0.16 | 3.0E-5 | 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 |
| 57 | hsa-miR-20a-5p | CDKN1A | 2.65 | 0 | -0.99 | 0 | miRNAWalker2 validate; miRTarBase; MirTarget; miRNATAP | -0.14 | 7.0E-5 | 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 |
| 58 | hsa-miR-28-5p | CDKN1A | 1.2 | 0 | -0.99 | 0 | miRNAWalker2 validate; miRTarBase; MirTarget; miRanda; miRNATAP | -0.2 | 0.00151 | NA | |
| 59 | hsa-miR-93-5p | CDKN1A | 1.51 | 0 | -0.99 | 0 | miRNAWalker2 validate; miRTarBase; MirTarget; miRNATAP | -0.17 | 6.0E-5 | 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 |
| 60 | hsa-miR-96-5p | CDKN1A | 3.04 | 0 | -0.99 | 0 | miRNAWalker2 validate; miRTarBase | -0.15 | 1.0E-5 | 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 |
| 61 | hsa-miR-98-5p | CDKN1A | 1.17 | 0 | -0.99 | 0 | miRNAWalker2 validate; MirTarget | -0.1 | 0.024 | NA | |
| 62 | hsa-miR-195-5p | CHEK1 | -1.02 | 5.0E-5 | 1.85 | 0 | MirTarget; miRNATAP | -0.35 | 0 | 25840419 | MiR 195 suppresses non small cell lung cancer by targeting CHEK1; We discovered that CHEK1 was a direct target of miR-195 which decreased CHEK1 expression in lung cancer cells |
| 63 | hsa-miR-320a | CHEK1 | -0.96 | 0 | 1.85 | 0 | MirTarget; miRanda | -0.28 | 4.0E-5 | NA | |
| 64 | hsa-miR-497-5p | CHEK1 | -0.05 | 0.78621 | 1.85 | 0 | MirTarget; miRNATAP | -0.49 | 0 | 24464213 | Checkpoint kinase 1 is negatively regulated by miR 497 in hepatocellular carcinoma; In silico analysis showed that CHEK1 was a candidate target of miR-497 which was previously found to be downregulated in HCC by us; To test whether miR-497 could bind to 3'untranslated region 3'UTR of CHEK1 luciferase reporter assay was conducted; The result revealed that miR-497 could bind to the 3'untranslated region 3'UTR of CHEK1 mRNA; Western blot showed that ectopic expression of miR-497 suppressed the CHEK1 expression and inhibition of miR-497 led to significant upregulation of CHEK1; Finally miR-497 expression was measured in the same 30 HCC samples and the correlation between miR-497 and CHEK1 was analyzed; The results indicated that miR-497 was downregulated in HCC and had a significant negative correlation with CHEK1; Taken together these results demonstrated that CHEK1 was negatively regulated by miR-497 and the overexpressed CHEK1 was resulted from the downregulated miR-497 in HCC which provided a potential molecular target for HCC therapy |
| 65 | hsa-miR-106a-5p | FAS | 1.39 | 6.0E-5 | -0.88 | 0.00034 | miRNAWalker2 validate; miRTarBase | -0.27 | 0 | 22431000; 27142596 | miR 106a is frequently upregulated in gastric cancer and inhibits the extrinsic apoptotic pathway by targeting FAS; Bioinformatic analysis combining with validation experiments identified FAS as a direct target of miR-106a; Moreover a significant inverse correlation was found between miR-106a and FAS expression not only in gastric cancer cell lines but also in gastric cancer specimens; Taken together these findings suggest that ectopicly overexpressed miR-106a may play an oncogenic role in gastric carcinogenesis and impair extrinsic apoptotic pathway through targeting FAS;Functional experiment ascertained that miR-106a interacted with FAS and mediated caspase3 pathway |
| 66 | hsa-miR-324-3p | GADD45B | -0.08 | 0.68923 | -1.59 | 0 | MirTarget; miRNATAP | -0.15 | 0.00558 | NA | |
| 67 | hsa-miR-127-3p | GADD45G | -0.72 | 0.01927 | 0.56 | 0.06996 | miRanda; miRNATAP | -0.18 | 0.00011 | NA | |
| 68 | hsa-miR-361-5p | IGF1 | 0.21 | 0.0801 | -0.88 | 0.00545 | PITA; mirMAP | -0.26 | 0.033 | NA | |
| 69 | hsa-miR-450b-5p | IGF1 | 1.69 | 0 | -0.88 | 0.00545 | MirTarget; PITA; mirMAP; miRNATAP | -0.16 | 0.00169 | NA | |
| 70 | hsa-miR-576-5p | IGF1 | 1.03 | 0 | -0.88 | 0.00545 | PITA; mirMAP; miRNATAP | -0.32 | 0 | NA | |
| 71 | hsa-miR-590-3p | IGF1 | 0.84 | 0.00129 | -0.88 | 0.00545 | MirTarget; miRanda; mirMAP; miRNATAP | -0.22 | 0.00113 | NA | |
| 72 | hsa-miR-374a-5p | IGFBP3 | -0.2 | 0.29808 | 1.35 | 3.0E-5 | MirTarget; mirMAP | -0.2 | 0.02606 | NA | |
| 73 | hsa-let-7a-5p | MDM4 | -1.37 | 0 | 0.5 | 0.00108 | MirTarget; TargetScan | -0.12 | 0.00218 | NA | |
| 74 | hsa-miR-361-5p | MDM4 | 0.21 | 0.0801 | 0.5 | 0.00108 | miRanda; mirMAP | -0.16 | 0.00809 | NA | |
| 75 | hsa-miR-200b-3p | PMAIP1 | 1.55 | 0 | 1.35 | 2.0E-5 | MirTarget; TargetScan | -0.25 | 0 | NA | |
| 76 | hsa-miR-200c-3p | PMAIP1 | 0.38 | 0.08422 | 1.35 | 2.0E-5 | miRNAWalker2 validate; miRTarBase; MirTarget | -0.31 | 0 | NA | |
| 77 | hsa-miR-15a-5p | PPM1D | 1.63 | 0 | -0.84 | 0 | MirTarget; miRNATAP | -0.2 | 0 | NA | |
| 78 | hsa-miR-29a-3p | PPM1D | 0.1 | 0.5732 | -0.84 | 0 | miRNAWalker2 validate; miRTarBase; MirTarget; miRNATAP | -0.13 | 1.0E-5 | NA | |
| 79 | hsa-miR-29b-3p | PPM1D | 3.11 | 0 | -0.84 | 0 | MirTarget; miRNATAP | -0.18 | 0 | NA | |
| 80 | hsa-miR-103a-3p | PTEN | 0.54 | 2.0E-5 | -0.42 | 0.00014 | miRNAWalker2 validate; miRTarBase | -0.18 | 1.0E-5 | 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 |
| 81 | hsa-miR-106b-5p | PTEN | 1.47 | 0 | -0.42 | 0.00014 | miRNAWalker2 validate; miRTarBase; miRNATAP | -0.1 | 3.0E-5 | 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 |
| 82 | hsa-miR-130a-3p | PTEN | 0.88 | 0.00016 | -0.42 | 0.00014 | MirTarget; miRNATAP | -0.1 | 0 | 24490491; 27062783; 22614869; 26837847; 27040383; 27035216; 26043084 | Down-regulated miR-130a did not affect cell proliferations but enhanced the sensitivity of the cells to cisplatin inhibited the expressions of MDR1 mRNA and P-gp and increased the expression of PTEN proteins; MiR-130a inhibitor can reverse the cisplatin resistance by upregulating the expression of PTEN proteins and down-regulating P-gp in A2780 cell lines;Platinum-resistant patients had significantly higher levels of expression of miR-130a and BCL-2 and lower level of PTEN than platinum-sensitive patients P < 0.05; MiR-130a may mediate the generation of platinum resistance in epithelial ovarian cancer through inhibiting PTEN to activate PI3K/AKT signaling pathway and increasing BCL-2 to inhibit tumor cell apoptosis;We found that miR-130a was upregulated in SKOV3/CIS compared to the parental SKOV3 cells and PTEN was predicted to be the potential target of miR-130a;The miR 130 family promotes cell migration and invasion in bladder cancer through FAK and Akt phosphorylation by regulating PTEN; In clinical bladder cancer specimens downregulation of PTEN was found to be closely correlated with miR-130 family expression levels;In addition by targeting PTEN 3' untranslated region miR-130a might increase cell growth and initiate protein kinase B AKT pathway activation;MicroRNA 130a promotes the metastasis and epithelial mesenchymal transition of osteosarcoma by targeting PTEN; MiR-130a exerted promoting effects on metastatic behavior and EMT of osteosarcoma cells through suppressing PTEN expression;This role of miR-130a may be achieved by regulating the MDR1 and PTEN gene expression |
| 83 | hsa-miR-130b-3p | PTEN | 1.83 | 0 | -0.42 | 0.00014 | MirTarget; miRNATAP | -0.11 | 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 |
| 84 | hsa-miR-141-3p | PTEN | 3.37 | 0 | -0.42 | 0.00014 | miRNAWalker2 validate; miRTarBase; TargetScan; miRNATAP | -0.1 | 0 | 27644195; 24742567 | Involvement of microRNA 141 3p in 5 fluorouracil and oxaliplatin chemo resistance in esophageal cancer cells via regulation of PTEN; Western blot exhibited altered protein levels of PTEN Akt and PI3k with miR-141-3p inhibitor; An inverse correlation between PTEN expression and miR-141-3p expression was also observed in tissue samples; Our study demonstrated that miR-141-3p contributed to an acquired chemo-resistance through PTEN modulation both in vitro and in vivo;PTEN might be a potential target of miR-141 and miR-200a in endometrial carcinogenesis |
| 85 | hsa-miR-148b-3p | PTEN | 0.48 | 0.00265 | -0.42 | 0.00014 | MirTarget; miRNATAP | -0.13 | 3.0E-5 | NA | |
| 86 | hsa-miR-17-5p | PTEN | 2.07 | 0 | -0.42 | 0.00014 | miRNAWalker2 validate; miRTarBase; TargetScan; miRNATAP | -0.19 | 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 |
| 87 | hsa-miR-186-5p | PTEN | 0.85 | 0 | -0.42 | 0.00014 | mirMAP; miRNATAP | -0.19 | 0 | NA | |
| 88 | hsa-miR-18a-5p | PTEN | 1.37 | 1.0E-5 | -0.42 | 0.00014 | miRNAWalker2 validate; miRTarBase | -0.14 | 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 |
| 89 | hsa-miR-193a-3p | PTEN | 0.55 | 0.0319 | -0.42 | 0.00014 | PITA; miRanda | -0.1 | 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 |
| 90 | hsa-miR-19a-3p | PTEN | 2.12 | 0 | -0.42 | 0.00014 | miRNAWalker2 validate; miRTarBase; MirTarget; miRNATAP | -0.15 | 0 | 26098000; 27289489; 27445062; 24831732; 21853360; 24681249; 25107371 | Moreover siRNA-mediated knockdown of PTEN a target of miR-19 also resulted in EMT migration and invasion of A549 and HCC827 cells suggesting that PTEN is involved in miR-19-induced EMT migration and invasion of lung cancer cells;Transfection of miR-19a and -19b mimics reversed the up-regulations of IGF2R and PTEN gene expression and abrogated the GSE induced anti-proliferative response;The target genes of miR-19a such as ABCA1 and PTEN that had been suppressed by miR recovered their expression through CAP treatment;Meanwhile BPA-induced upregulation of oncogenic miR-19a and miR-19b and the dysregulated expression of miR-19-related downstream proteins including PTEN p-AKT p-MDM2 p53 and proliferating cell nuclear antigen were reversed by curcumin;Regulation of miR 19 to breast cancer chemoresistance through targeting PTEN; Expression levels of miR-19 in MDR cells were inversely consistent with those of PTEN; Our findings demonstrate for the first time involvement of miR-19 in multidrug resistance through modulation of PTEN and suggest that miR-19 may be a potential target for preventing and reversing MDR in tumor cells;miR-19 in the context of the miR-17~92 cluster at medium levels promoted tumor metastasis through induction of Wnt/β-catenin-mediated epithelial-mesenchymal transition by targeting to the tumor-suppressor gene PTEN;The target of miR-19a was identified by western blot and whether its regulatory role depends on its target was improved by a rescue experiment with miR-19a mimic and PTEN expression plasmid; Meanwhile gain or loss of function of miR-19a demonstrated that miR-19a can promote cell growth of bladder cancer cells and the further mechanism studies indicated that its oncogenic role was dependent on targeting PTEN; The oncogenic role of miR19a in bladder cancer was dependent on targeting PTEN |
| 91 | hsa-miR-19b-3p | PTEN | 2.11 | 0 | -0.42 | 0.00014 | miRNAWalker2 validate; miRTarBase; MirTarget; miRNATAP | -0.14 | 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 |
| 92 | hsa-miR-20a-5p | PTEN | 2.65 | 0 | -0.42 | 0.00014 | miRNAWalker2 validate; miRTarBase; miRNATAP | -0.16 | 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 |
| 93 | hsa-miR-25-3p | PTEN | 0.36 | 0.01637 | -0.42 | 0.00014 | miRTarBase; MirTarget; miRNATAP | -0.12 | 0.00041 | NA | |
| 94 | hsa-miR-26b-5p | PTEN | 0.72 | 5.0E-5 | -0.42 | 0.00014 | MirTarget; miRNATAP | -0.1 | 0.00034 | 26068649 | Down regulation of microRNA 26b modulates non small cell lung cancer cells chemoresistance and migration through the association of PTEN; It indicates that miR-26b may regulate NSCLC migration and chemosensitivity through the regulation of PTEN |
| 95 | hsa-miR-301a-3p | PTEN | 2.7 | 0 | -0.42 | 0.00014 | MirTarget; miRNATAP | -0.14 | 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 |
| 96 | hsa-miR-454-3p | PTEN | 1.49 | 0 | -0.42 | 0.00014 | MirTarget; miRNATAP | -0.21 | 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 |
| 97 | hsa-miR-92a-3p | PTEN | -0.14 | 0.49341 | -0.42 | 0.00014 | MirTarget; miRNATAP | -0.12 | 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 |
| 98 | hsa-miR-93-5p | PTEN | 1.51 | 0 | -0.42 | 0.00014 | miRNAWalker2 validate; miRTarBase; miRNATAP | -0.21 | 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 |
| 99 | hsa-let-7a-5p | RRM2 | -1.37 | 0 | 2.87 | 0 | miRNAWalker2 validate; TargetScan; miRNATAP | -0.58 | 0 | NA | |
| 100 | hsa-let-7b-5p | RRM2 | -1.62 | 0 | 2.87 | 0 | miRNAWalker2 validate; miRNATAP | -0.64 | 0 | NA | |
| 101 | hsa-let-7g-5p | RRM2 | 0.08 | 0.58308 | 2.87 | 0 | miRNAWalker2 validate; miRNATAP | -0.31 | 0.0021 | NA | |
| 102 | hsa-miR-142-3p | RRM2B | 3.98 | 0 | -0.56 | 0.00033 | miRNAWalker2 validate; miRanda | -0.12 | 0 | NA | |
| 103 | hsa-miR-590-5p | RRM2B | 2.07 | 0 | -0.56 | 0.00033 | miRanda; mirMAP | -0.28 | 0 | NA | |
| 104 | hsa-miR-30c-5p | SERPINE1 | -0.33 | 0.1236 | -0.11 | 0.73683 | miRNAWalker2 validate; miRTarBase; MirTarget; miRNATAP | -0.28 | 0.00011 | NA | |
| 105 | hsa-miR-15a-5p | SESN1 | 1.63 | 0 | -1.81 | 0 | MirTarget; miRNATAP | -0.15 | 0.00123 | NA | |
| 106 | hsa-miR-28-5p | SESN1 | 1.2 | 0 | -1.81 | 0 | PITA; miRanda; miRNATAP | -0.21 | 0.001 | NA | |
| 107 | hsa-miR-424-5p | SESN1 | 1.26 | 1.0E-5 | -1.81 | 0 | MirTarget; miRNATAP | -0.12 | 0.00012 | NA | |
| 108 | hsa-miR-17-5p | SESN3 | 2.07 | 0 | -0.1 | 0.73838 | MirTarget; TargetScan | -0.32 | 0 | NA | |
| 109 | hsa-miR-25-3p | SESN3 | 0.36 | 0.01637 | -0.1 | 0.73838 | MirTarget; miRNATAP | -0.26 | 0.0033 | NA | |
| 110 | hsa-miR-29a-5p | SESN3 | 1.9 | 0 | -0.1 | 0.73838 | MirTarget; mirMAP | -0.22 | 9.0E-5 | NA | |
| 111 | hsa-miR-32-5p | SESN3 | 0.88 | 6.0E-5 | -0.1 | 0.73838 | MirTarget; miRNATAP | -0.14 | 0.03723 | NA | |
| 112 | hsa-miR-320b | SESN3 | 0.23 | 0.37882 | -0.1 | 0.73838 | miRanda; mirMAP | -0.17 | 0.00129 | NA | |
| 113 | hsa-miR-589-3p | SESN3 | 1.34 | 2.0E-5 | -0.1 | 0.73838 | MirTarget; mirMAP | -0.11 | 0.00909 | NA | |
| 114 | hsa-miR-590-3p | SESN3 | 0.84 | 0.00129 | -0.1 | 0.73838 | miRNAWalker2 validate; MirTarget; miRanda | -0.28 | 1.0E-5 | NA | |
| 115 | hsa-miR-7-1-3p | SESN3 | 2.61 | 0 | -0.1 | 0.73838 | MirTarget; mirMAP | -0.19 | 0.0011 | NA | |
| 116 | hsa-miR-92a-3p | SESN3 | -0.14 | 0.49341 | -0.1 | 0.73838 | MirTarget; miRNATAP | -0.26 | 9.0E-5 | NA | |
| 117 | hsa-miR-96-5p | SESN3 | 3.04 | 0 | -0.1 | 0.73838 | MirTarget; TargetScan | -0.19 | 0.00013 | NA | |
| 118 | hsa-miR-19a-3p | THBS1 | 2.12 | 0 | -0.93 | 0.0014 | MirTarget; mirMAP | -0.32 | 0 | NA | |
| 119 | hsa-miR-19b-3p | THBS1 | 2.11 | 0 | -0.93 | 0.0014 | MirTarget; mirMAP | -0.39 | 0 | NA | |
| 120 | hsa-miR-338-3p | THBS1 | 0.73 | 0.05063 | -0.93 | 0.0014 | MirTarget; PITA; miRanda | -0.14 | 0.00014 | NA | |
| 121 | hsa-miR-590-5p | THBS1 | 2.07 | 0 | -0.93 | 0.0014 | miRanda; mirMAP | -0.25 | 3.0E-5 | NA | |
| 122 | hsa-miR-7-1-3p | THBS1 | 2.61 | 0 | -0.93 | 0.0014 | MirTarget; mirMAP | -0.3 | 0 | NA | |
| 123 | hsa-miR-429 | ZMAT3 | 2.38 | 0 | -0.32 | 0.07814 | MirTarget; miRNATAP | -0.1 | 0.00011 | NA | |
| 124 | hsa-miR-501-5p | ZMAT3 | 0.41 | 0.10435 | -0.32 | 0.07814 | MirTarget; mirMAP | -0.22 | 0 | NA | |
| 125 | hsa-miR-590-3p | ZMAT3 | 0.84 | 0.00129 | -0.32 | 0.07814 | mirMAP; miRNATAP | -0.14 | 0.00018 | NA |
| Num | GO | Overlap | Size | P Value | Adj. P Value |
|---|---|---|---|---|---|
| 1 | REGULATION OF CELL CYCLE | 19 | 949 | 2.729e-19 | 1.27e-15 |
| 2 | CELL CYCLE | 17 | 1316 | 7.892e-14 | 1.836e-10 |
| 3 | REGULATION OF CYCLIN DEPENDENT PROTEIN KINASE ACTIVITY | 8 | 97 | 6.544e-13 | 1.015e-09 |
| 4 | CELL CYCLE PROCESS | 15 | 1081 | 1.721e-12 | 2.002e-09 |
| 5 | REGULATION OF PROTEIN MODIFICATION PROCESS | 17 | 1710 | 5.568e-12 | 5.182e-09 |
| 6 | MITOTIC CELL CYCLE | 13 | 766 | 7.593e-12 | 5.889e-09 |
| 7 | REGULATION OF KINASE ACTIVITY | 13 | 776 | 8.935e-12 | 5.939e-09 |
| 8 | REGULATION OF PROTEIN SERINE THREONINE KINASE ACTIVITY | 11 | 470 | 1.61e-11 | 9.362e-09 |
| 9 | REGULATION OF PHOSPHORUS METABOLIC PROCESS | 16 | 1618 | 3.736e-11 | 1.931e-08 |
| 10 | CELL CYCLE PHASE TRANSITION | 9 | 255 | 4.323e-11 | 2.012e-08 |
| 11 | REGULATION OF TRANSFERASE ACTIVITY | 13 | 946 | 1.057e-10 | 4.47e-08 |
| 12 | CELL CYCLE G1 S PHASE TRANSITION | 7 | 111 | 1.44e-10 | 4.787e-08 |
| 13 | G1 S TRANSITION OF MITOTIC CELL CYCLE | 7 | 111 | 1.44e-10 | 4.787e-08 |
| 14 | REGULATION OF CELL DEATH | 15 | 1472 | 1.408e-10 | 4.787e-08 |
| 15 | REGULATION OF CELL PROLIFERATION | 15 | 1496 | 1.769e-10 | 5.487e-08 |
| 16 | NEGATIVE REGULATION OF CELL CYCLE | 10 | 433 | 1.89e-10 | 5.496e-08 |
| 17 | RESPONSE TO OXYGEN LEVELS | 9 | 311 | 2.524e-10 | 6.524e-08 |
| 18 | POSITIVE REGULATION OF CELL DEATH | 11 | 605 | 2.386e-10 | 6.524e-08 |
| 19 | POSITIVE REGULATION OF PROTEIN METABOLIC PROCESS | 14 | 1492 | 2.307e-09 | 5.65e-07 |
| 20 | RESPONSE TO ABIOTIC STIMULUS | 12 | 1024 | 4.323e-09 | 1.006e-06 |
| 21 | CELL DIVISION | 9 | 460 | 7.806e-09 | 1.73e-06 |
| 22 | NEGATIVE REGULATION OF CELL PROLIFERATION | 10 | 643 | 8.557e-09 | 1.81e-06 |
| 23 | REGULATION OF EXTRINSIC APOPTOTIC SIGNALING PATHWAY VIA DEATH DOMAIN RECEPTORS | 5 | 55 | 1.223e-08 | 2.392e-06 |
| 24 | POSITIVE REGULATION OF CELL CYCLE | 8 | 332 | 1.234e-08 | 2.392e-06 |
| 25 | RESPONSE TO STEROID HORMONE | 9 | 497 | 1.525e-08 | 2.839e-06 |
| 26 | RESPONSE TO ALCOHOL | 8 | 362 | 2.416e-08 | 4.324e-06 |
| 27 | CELLULAR RESPONSE TO STRESS | 13 | 1565 | 4.813e-08 | 8.295e-06 |
| 28 | REGULATION OF EXTRINSIC APOPTOTIC SIGNALING PATHWAY | 6 | 153 | 5.955e-08 | 9.896e-06 |
| 29 | POSITIVE REGULATION OF PHOSPHATE METABOLIC PROCESS | 11 | 1036 | 6.502e-08 | 1.008e-05 |
| 30 | POSITIVE REGULATION OF PHOSPHORUS METABOLIC PROCESS | 11 | 1036 | 6.502e-08 | 1.008e-05 |
| 31 | REGENERATION | 6 | 161 | 8.064e-08 | 1.194e-05 |
| 32 | RESPONSE TO X RAY | 4 | 30 | 8.212e-08 | 1.194e-05 |
| 33 | REGULATION OF FIBROBLAST PROLIFERATION | 5 | 81 | 8.783e-08 | 1.238e-05 |
| 34 | RESPONSE TO DRUG | 8 | 431 | 9.283e-08 | 1.27e-05 |
| 35 | ORGAN REGENERATION | 5 | 83 | 9.934e-08 | 1.321e-05 |
| 36 | RESPONSE TO CORTICOSTEROID | 6 | 176 | 1.368e-07 | 1.768e-05 |
| 37 | RESPONSE TO KETONE | 6 | 182 | 1.668e-07 | 2.042e-05 |
| 38 | POSITIVE REGULATION OF PROTEIN MODIFICATION PROCESS | 11 | 1135 | 1.644e-07 | 2.042e-05 |
| 39 | RESPONSE TO LIPID | 10 | 888 | 1.791e-07 | 2.083e-05 |
| 40 | POSITIVE REGULATION OF CYCLIN DEPENDENT PROTEIN KINASE ACTIVITY | 4 | 36 | 1.755e-07 | 2.083e-05 |
| 41 | POSITIVE REGULATION OF MOLECULAR FUNCTION | 13 | 1791 | 2.361e-07 | 2.631e-05 |
| 42 | RESPONSE TO ORGANIC CYCLIC COMPOUND | 10 | 917 | 2.414e-07 | 2.631e-05 |
| 43 | CELL CYCLE CHECKPOINT | 6 | 194 | 2.432e-07 | 2.631e-05 |
| 44 | POSITIVE REGULATION OF CATALYTIC ACTIVITY | 12 | 1518 | 3.383e-07 | 3.578e-05 |
| 45 | CELLULAR RESPONSE TO DNA DAMAGE STIMULUS | 9 | 720 | 3.608e-07 | 3.707e-05 |
| 46 | DNA REPLICATION | 6 | 208 | 3.664e-07 | 3.707e-05 |
| 47 | NEGATIVE REGULATION OF CELL CYCLE PROCESS | 6 | 214 | 4.33e-07 | 4.287e-05 |
| 48 | RESPONSE TO ESTROGEN | 6 | 218 | 4.827e-07 | 4.679e-05 |
| 49 | REGULATION OF APOPTOTIC SIGNALING PATHWAY | 7 | 363 | 5.221e-07 | 4.958e-05 |
| 50 | CELL DEATH | 10 | 1001 | 5.421e-07 | 5.045e-05 |
| 51 | RESPONSE TO UV | 5 | 126 | 8.018e-07 | 7.315e-05 |
| 52 | POSITIVE REGULATION OF FIBROBLAST PROLIFERATION | 4 | 53 | 8.582e-07 | 7.535e-05 |
| 53 | POSITIVE REGULATION OF EXTRINSIC APOPTOTIC SIGNALING PATHWAY | 4 | 53 | 8.582e-07 | 7.535e-05 |
| 54 | POSITIVE REGULATION OF CELL CYCLE PROCESS | 6 | 247 | 1.002e-06 | 8.632e-05 |
| 55 | POSITIVE REGULATION OF TRANSFERASE ACTIVITY | 8 | 616 | 1.394e-06 | 0.000118 |
| 56 | CELLULAR RESPONSE TO EXTERNAL STIMULUS | 6 | 264 | 1.475e-06 | 0.0001204 |
| 57 | AGING | 6 | 264 | 1.475e-06 | 0.0001204 |
| 58 | RESPONSE TO NITROGEN COMPOUND | 9 | 859 | 1.576e-06 | 0.0001264 |
| 59 | RESPONSE TO ESTRADIOL | 5 | 146 | 1.661e-06 | 0.0001288 |
| 60 | POSITIVE REGULATION OF EXTRINSIC APOPTOTIC SIGNALING PATHWAY VIA DEATH DOMAIN RECEPTORS | 3 | 17 | 1.649e-06 | 0.0001288 |
| 61 | NEGATIVE REGULATION OF CELL DEATH | 9 | 872 | 1.785e-06 | 0.0001361 |
| 62 | RESPONSE TO EXTRACELLULAR STIMULUS | 7 | 441 | 1.916e-06 | 0.0001438 |
| 63 | RESPONSE TO HORMONE | 9 | 893 | 2.173e-06 | 0.000158 |
| 64 | REGULATION OF RESPONSE TO STRESS | 11 | 1468 | 2.143e-06 | 0.000158 |
| 65 | RESPONSE TO EXTERNAL STIMULUS | 12 | 1821 | 2.38e-06 | 0.0001703 |
| 66 | POSITIVE REGULATION OF PROTEIN SERINE THREONINE KINASE ACTIVITY | 6 | 289 | 2.492e-06 | 0.0001757 |
| 67 | NEGATIVE REGULATION OF CELL CYCLE ARREST | 3 | 20 | 2.757e-06 | 0.0001915 |
| 68 | REGULATION OF MITOTIC CELL CYCLE | 7 | 468 | 2.841e-06 | 0.0001944 |
| 69 | POSITIVE REGULATION OF MAPK CASCADE | 7 | 470 | 2.922e-06 | 0.000197 |
| 70 | POSITIVE REGULATION OF KINASE ACTIVITY | 7 | 482 | 3.451e-06 | 0.0002294 |
| 71 | RESPONSE TO INCREASED OXYGEN LEVELS | 3 | 23 | 4.271e-06 | 0.000276 |
| 72 | RESPONSE TO HYPEROXIA | 3 | 23 | 4.271e-06 | 0.000276 |
| 73 | RESPONSE TO METAL ION | 6 | 333 | 5.632e-06 | 0.000359 |
| 74 | RESPONSE TO CORTICOSTERONE | 3 | 26 | 6.253e-06 | 0.0003932 |
| 75 | REGULATION OF INTRACELLULAR SIGNAL TRANSDUCTION | 11 | 1656 | 6.928e-06 | 0.0004298 |
| 76 | REGULATION OF CELL MATRIX ADHESION | 4 | 90 | 7.227e-06 | 0.0004425 |
| 77 | NEGATIVE REGULATION OF MITOTIC CELL CYCLE | 5 | 199 | 7.566e-06 | 0.0004572 |
| 78 | NEGATIVE REGULATION OF APOPTOTIC SIGNALING PATHWAY | 5 | 200 | 7.753e-06 | 0.0004625 |
| 79 | REGULATION OF CELL CYCLE PROCESS | 7 | 558 | 9.012e-06 | 0.0005308 |
| 80 | NEGATIVE REGULATION OF CELL MATRIX ADHESION | 3 | 30 | 9.727e-06 | 0.0005658 |
| 81 | NEGATIVE REGULATION OF EXTRINSIC APOPTOTIC SIGNALING PATHWAY | 4 | 98 | 1.014e-05 | 0.0005684 |
| 82 | RESPONSE TO OXYGEN CONTAINING COMPOUND | 10 | 1381 | 9.899e-06 | 0.0005684 |
| 83 | NEGATIVE REGULATION OF CELL CYCLE G1 S PHASE TRANSITION | 4 | 98 | 1.014e-05 | 0.0005684 |
| 84 | NEGATIVE REGULATION OF CYCLIN DEPENDENT PROTEIN KINASE ACTIVITY | 3 | 32 | 1.186e-05 | 0.000657 |
| 85 | T CELL HOMEOSTASIS | 3 | 34 | 1.428e-05 | 0.0007819 |
| 86 | REGULATION OF CELL CYCLE ARREST | 4 | 108 | 1.49e-05 | 0.0008061 |
| 87 | RESPONSE TO ENDOGENOUS STIMULUS | 10 | 1450 | 1.521e-05 | 0.0008134 |
| 88 | RESPONSE TO MINERALOCORTICOID | 3 | 35 | 1.561e-05 | 0.0008253 |
| 89 | POSITIVE REGULATION OF INTRACELLULAR SIGNAL TRANSDUCTION | 8 | 876 | 1.865e-05 | 0.0009751 |
| 90 | RESPONSE TO RADIATION | 6 | 413 | 1.916e-05 | 0.0009907 |
| 91 | POSITIVE REGULATION OF MITOTIC CELL CYCLE | 4 | 123 | 2.488e-05 | 0.001272 |
| 92 | REGULATION OF MAPK CASCADE | 7 | 660 | 2.669e-05 | 0.00135 |
| 93 | SIGNAL TRANSDUCTION BY P53 CLASS MEDIATOR | 4 | 127 | 2.821e-05 | 0.001411 |
| 94 | PROTEIN STABILIZATION | 4 | 131 | 3.186e-05 | 0.001577 |
| 95 | REGULATION OF CELLULAR RESPONSE TO STRESS | 7 | 691 | 3.58e-05 | 0.001753 |
| 96 | PHOSPHATE CONTAINING COMPOUND METABOLIC PROCESS | 11 | 1977 | 3.735e-05 | 0.00181 |
| 97 | CIRCADIAN RHYTHM | 4 | 137 | 3.797e-05 | 0.001821 |
| 98 | RESPONSE TO LIGHT STIMULUS | 5 | 280 | 3.917e-05 | 0.00186 |
| 99 | REGULATION OF EPITHELIAL CELL PROLIFERATION | 5 | 285 | 4.262e-05 | 0.002003 |
| 100 | REGULATION OF SMOOTH MUSCLE CELL MIGRATION | 3 | 49 | 4.336e-05 | 0.002018 |
| 101 | RESPONSE TO INORGANIC SUBSTANCE | 6 | 479 | 4.402e-05 | 0.002028 |
| 102 | CELLULAR RESPONSE TO OXYGEN LEVELS | 4 | 143 | 4.49e-05 | 0.002048 |
| 103 | APOPTOTIC SIGNALING PATHWAY | 5 | 289 | 4.554e-05 | 0.002057 |
| 104 | LYMPHOCYTE HOMEOSTASIS | 3 | 50 | 4.609e-05 | 0.002062 |
| 105 | RESPONSE TO IONIZING RADIATION | 4 | 145 | 4.74e-05 | 0.0021 |
| 106 | NEGATIVE REGULATION OF CELL CYCLE PHASE TRANSITION | 4 | 146 | 4.869e-05 | 0.002117 |
| 107 | DNA INTEGRITY CHECKPOINT | 4 | 146 | 4.869e-05 | 0.002117 |
| 108 | REGULATION OF CELL CYCLE G1 S PHASE TRANSITION | 4 | 147 | 5e-05 | 0.002154 |
| 109 | RHYTHMIC PROCESS | 5 | 298 | 5.268e-05 | 0.002249 |
| 110 | NEGATIVE REGULATION OF CELL SUBSTRATE ADHESION | 3 | 53 | 5.493e-05 | 0.002303 |
| 111 | INTRINSIC APOPTOTIC SIGNALING PATHWAY BY P53 CLASS MEDIATOR | 3 | 53 | 5.493e-05 | 0.002303 |
| 112 | CELL CYCLE ARREST | 4 | 154 | 5.994e-05 | 0.00249 |
| 113 | NEGATIVE REGULATION OF RESPONSE TO STIMULUS | 9 | 1360 | 6.404e-05 | 0.002629 |
| 114 | DNA METABOLIC PROCESS | 7 | 758 | 6.442e-05 | 0.002629 |
| 115 | REGULATION OF SIGNAL TRANSDUCTION BY P53 CLASS MEDIATOR | 4 | 162 | 7.297e-05 | 0.002953 |
| 116 | REGULATION OF CELL CYCLE PHASE TRANSITION | 5 | 321 | 7.491e-05 | 0.003005 |
| 117 | REGULATION OF EPITHELIAL CELL APOPTOTIC PROCESS | 3 | 59 | 7.58e-05 | 0.003015 |
| 118 | LEUKOCYTE HOMEOSTASIS | 3 | 60 | 7.972e-05 | 0.003143 |
| 119 | RESPONSE TO CARBOHYDRATE | 4 | 168 | 8.403e-05 | 0.003286 |
| 120 | NEGATIVE REGULATION OF PROTEIN METABOLIC PROCESS | 8 | 1087 | 8.69e-05 | 0.00337 |
| 121 | POSITIVE REGULATION OF APOPTOTIC SIGNALING PATHWAY | 4 | 171 | 8.999e-05 | 0.003461 |
| 122 | REGULATION OF CELL SUBSTRATE ADHESION | 4 | 173 | 9.413e-05 | 0.00359 |
| 123 | ACTIVATION OF MAPKKK ACTIVITY | 2 | 11 | 0.0001031 | 0.003902 |
| 124 | CELL AGING | 3 | 67 | 0.0001109 | 0.00416 |
| 125 | POSITIVE REGULATION OF CELL CYCLE PHASE TRANSITION | 3 | 68 | 0.0001159 | 0.004313 |
| 126 | DEOXYRIBONUCLEOTIDE BIOSYNTHETIC PROCESS | 2 | 12 | 0.0001237 | 0.004496 |
| 127 | REPLICATIVE SENESCENCE | 2 | 12 | 0.0001237 | 0.004496 |
| 128 | POSITIVE REGULATION OF INSULIN LIKE GROWTH FACTOR RECEPTOR SIGNALING PATHWAY | 2 | 12 | 0.0001237 | 0.004496 |
| 129 | CELLULAR RESPONSE TO EXTRACELLULAR STIMULUS | 4 | 188 | 0.0001298 | 0.00468 |
| 130 | RESPONSE TO NUTRIENT | 4 | 191 | 0.0001379 | 0.004936 |
| 131 | HIPPOCAMPUS DEVELOPMENT | 3 | 73 | 0.0001431 | 0.005045 |
| 132 | G1 DNA DAMAGE CHECKPOINT | 3 | 73 | 0.0001431 | 0.005045 |
| 133 | RESPONSE TO COBALT ION | 2 | 13 | 0.000146 | 0.005109 |
| 134 | NEGATIVE REGULATION OF CELL COMMUNICATION | 8 | 1192 | 0.0001653 | 0.00574 |
| 135 | REGULATION OF FIBRINOLYSIS | 2 | 14 | 0.0001702 | 0.005805 |
| 136 | POSITIVE REGULATION OF P38MAPK CASCADE | 2 | 14 | 0.0001702 | 0.005805 |
| 137 | RESPONSE TO BIOTIC STIMULUS | 7 | 886 | 0.0001709 | 0.005805 |
| 138 | REGULATION OF PEPTIDASE ACTIVITY | 5 | 392 | 0.0001911 | 0.006443 |
| 139 | DENTATE GYRUS DEVELOPMENT | 2 | 15 | 0.0001962 | 0.006502 |
| 140 | RESPONSE TO VITAMIN E | 2 | 15 | 0.0001962 | 0.006502 |
| 141 | REGULATION OF CELL ADHESION | 6 | 629 | 0.000197 | 0.006502 |
| 142 | REGULATION OF CYSTEINE TYPE ENDOPEPTIDASE ACTIVITY | 4 | 213 | 0.0002095 | 0.006866 |
| 143 | NEGATIVE REGULATION OF ADHERENS JUNCTION ORGANIZATION | 2 | 16 | 0.0002241 | 0.00724 |
| 144 | NEGATIVE REGULATION OF SMOOTH MUSCLE CELL MIGRATION | 2 | 16 | 0.0002241 | 0.00724 |
| 145 | REGULATION OF PROTEIN STABILITY | 4 | 221 | 0.0002412 | 0.007741 |
| 146 | NEGATIVE REGULATION OF CELL ADHESION | 4 | 223 | 0.0002497 | 0.007956 |
| 147 | NEGATIVE REGULATION OF CELL AGING | 2 | 17 | 0.0002537 | 0.007977 |
| 148 | PROTEIN PHOSPHORYLATION | 7 | 944 | 0.0002526 | 0.007977 |
| 149 | RESPONSE TO HEAT | 3 | 89 | 0.0002575 | 0.00804 |
| 150 | NEGATIVE REGULATION OF PHOSPHORYLATION | 5 | 422 | 0.0002689 | 0.008341 |
| 151 | TELENCEPHALON DEVELOPMENT | 4 | 228 | 0.0002717 | 0.008371 |
| 152 | CELL PROLIFERATION | 6 | 672 | 0.0002816 | 0.008621 |
| 153 | POSITIVE REGULATION OF CELL CYCLE G2 M PHASE TRANSITION | 2 | 18 | 0.0002852 | 0.008673 |
| 154 | ACTIVATION OF CYSTEINE TYPE ENDOPEPTIDASE ACTIVITY | 3 | 95 | 0.000312 | 0.009428 |
| 155 | LIVER REGENERATION | 2 | 19 | 0.0003185 | 0.009561 |
| Num | GO | Overlap | Size | P Value | Adj. P Value |
|---|---|---|---|---|---|
| 1 | CYCLIN DEPENDENT PROTEIN SERINE THREONINE KINASE REGULATOR ACTIVITY | 6 | 28 | 1.565e-12 | 1.454e-09 |
| 2 | KINASE REGULATOR ACTIVITY | 6 | 186 | 1.897e-07 | 8.81e-05 |
| 3 | KINASE BINDING | 8 | 606 | 1.233e-06 | 0.0003347 |
| 4 | ENZYME BINDING | 12 | 1737 | 1.441e-06 | 0.0003347 |
| 5 | CYCLIN BINDING | 3 | 19 | 2.346e-06 | 0.0004358 |
| 6 | PROTEIN COMPLEX BINDING | 9 | 935 | 3.172e-06 | 0.0004911 |
| 7 | CYCLIN DEPENDENT PROTEIN KINASE ACTIVITY | 3 | 34 | 1.428e-05 | 0.001896 |
| 8 | ENZYME REGULATOR ACTIVITY | 8 | 959 | 3.576e-05 | 0.004152 |
| 9 | MACROMOLECULAR COMPLEX BINDING | 9 | 1399 | 7.981e-05 | 0.008238 |
| Num | GO | Overlap | Size | P Value | Adj. P Value |
|---|---|---|---|---|---|
| 1 | CYCLIN DEPENDENT PROTEIN KINASE HOLOENZYME COMPLEX | 7 | 31 | 1.2e-14 | 7.011e-12 |
| 2 | PROTEIN KINASE COMPLEX | 7 | 90 | 3.23e-11 | 9.433e-09 |
| 3 | TRANSFERASE COMPLEX TRANSFERRING PHOSPHORUS CONTAINING GROUPS | 7 | 237 | 2.876e-08 | 5.599e-06 |
| 4 | CATALYTIC COMPLEX | 9 | 1038 | 7.443e-06 | 0.001087 |
| 5 | TRANSFERASE COMPLEX | 7 | 703 | 3.995e-05 | 0.004666 |
| 6 | PLATELET ALPHA GRANULE LUMEN | 3 | 55 | 6.14e-05 | 0.005976 |
Over-represented Pathway
| Num | Pathway | Pathview | Overlap | Size | P Value | Adj. P Value |
|---|---|---|---|---|---|---|
| 1 | p53_signaling_pathway_hsa04115 | 28 | 68 | 1.154e-72 | 6.001e-71 | |
| 2 | Cellular_senescence_hsa04218 | 14 | 160 | 8.968e-23 | 2.332e-21 | |
| 3 | Cell_cycle_hsa04110 | 11 | 124 | 6.498e-18 | 1.126e-16 | |
| 4 | PI3K_Akt_signaling_pathway_hsa04151 | 11 | 352 | 7.062e-13 | 9.18e-12 | |
| 5 | FoxO_signaling_pathway_hsa04068 | 8 | 132 | 8.082e-12 | 8.405e-11 | |
| 6 | Focal_adhesion_hsa04510 | 6 | 199 | 2.825e-07 | 2.448e-06 | |
| 7 | Apoptosis_hsa04210 | 5 | 138 | 1.258e-06 | 9.345e-06 | |
| 8 | MAPK_signaling_pathway_hsa04010 | 5 | 295 | 5.021e-05 | 0.0003264 | |
| 9 | Hippo_signaling_pathway_hsa04390 | 4 | 154 | 5.994e-05 | 0.0003463 | |
| 10 | Jak_STAT_signaling_pathway_hsa04630 | 4 | 162 | 7.297e-05 | 0.0003795 | |
| 11 | HIF_1_signaling_pathway_hsa04066 | 3 | 100 | 0.0003628 | 0.001715 | |
| 12 | Oocyte_meiosis_hsa04114 | 3 | 124 | 0.0006804 | 0.002949 | |
| 13 | Apoptosis_multiple_species_hsa04215 | 2 | 33 | 0.0009715 | 0.003886 | |
| 14 | Wnt_signaling_pathway_hsa04310 | 3 | 146 | 0.001092 | 0.004056 | |
| 15 | Hedgehog_signaling_pathway_hsa04340 | 2 | 47 | 0.001965 | 0.006812 | |
| 16 | TNF_signaling_pathway_hsa04668 | 2 | 108 | 0.009965 | 0.03239 | |
| 17 | AMPK_signaling_pathway_hsa04152 | 2 | 121 | 0.01238 | 0.03787 | |
| 18 | Apelin_signaling_pathway_hsa04371 | 2 | 137 | 0.01567 | 0.04527 | |
| 19 | mTOR_signaling_pathway_hsa04150 | 2 | 151 | 0.01882 | 0.05152 | |
| 20 | Tight_junction_hsa04530 | 2 | 170 | 0.02349 | 0.06108 | |
| 21 | Rap1_signaling_pathway_hsa04015 | 2 | 206 | 0.03348 | 0.08291 |
lncRNA-mediated sponge
| Num | lncRNA | miRNAs | miRNAs count | Gene | Sponge regulatory network | lncRNA log2FC | lncRNA pvalue | Gene log2FC | Gene pvalue | lncRNA-gene Pearson correlation |
|---|---|---|---|---|---|---|---|---|---|---|
| 1 | RP11-389C8.2 |
hsa-miR-106b-5p;hsa-miR-141-3p;hsa-miR-17-5p;hsa-miR-182-5p;hsa-miR-185-5p;hsa-miR-186-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-590-3p | 10 | CCND2 | Sponge network | -2.039 | 0 | -1.641 | 0 | 0.52 |
| 2 | LINC00702 |
hsa-miR-106b-5p;hsa-miR-141-3p;hsa-miR-15a-5p;hsa-miR-16-5p;hsa-miR-17-5p;hsa-miR-182-5p;hsa-miR-185-5p;hsa-miR-186-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-320b;hsa-miR-450b-5p;hsa-miR-501-5p;hsa-miR-590-3p;hsa-miR-96-5p | 16 | CCND2 | Sponge network | -2.856 | 0 | -1.641 | 0 | 0.433 |
| 3 | TBX5-AS1 |
hsa-miR-106b-5p;hsa-miR-141-3p;hsa-miR-15a-5p;hsa-miR-16-5p;hsa-miR-17-5p;hsa-miR-182-5p;hsa-miR-185-5p;hsa-miR-186-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-450b-5p;hsa-miR-501-5p | 13 | CCND2 | Sponge network | -2.108 | 0 | -1.641 | 0 | 0.404 |
| 4 | AC011899.9 |
hsa-miR-106b-5p;hsa-miR-141-3p;hsa-miR-16-5p;hsa-miR-17-5p;hsa-miR-182-5p;hsa-miR-186-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-590-3p | 10 | CCND2 | Sponge network | -2.611 | 0 | -1.641 | 0 | 0.404 |
| 5 | LINC00968 |
hsa-miR-106b-5p;hsa-miR-141-3p;hsa-miR-15a-5p;hsa-miR-16-5p;hsa-miR-17-5p;hsa-miR-182-5p;hsa-miR-185-5p;hsa-miR-186-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-320b;hsa-miR-450b-5p;hsa-miR-590-3p;hsa-miR-96-5p | 15 | CCND2 | Sponge network | -4.19 | 0 | -1.641 | 0 | 0.396 |
| 6 | MAGI2-AS3 |
hsa-miR-106b-5p;hsa-miR-141-3p;hsa-miR-15a-5p;hsa-miR-16-5p;hsa-miR-17-5p;hsa-miR-182-5p;hsa-miR-185-5p;hsa-miR-186-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-320b;hsa-miR-501-5p;hsa-miR-590-3p | 14 | CCND2 | Sponge network | -1.892 | 0 | -1.641 | 0 | 0.378 |
| 7 | RP11-1024P17.1 |
hsa-miR-106b-5p;hsa-miR-141-3p;hsa-miR-16-5p;hsa-miR-17-5p;hsa-miR-182-5p;hsa-miR-186-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-320b;hsa-miR-590-3p | 11 | CCND2 | Sponge network | -2.062 | 0 | -1.641 | 0 | 0.374 |
| 8 | RP11-1008C21.1 |
hsa-miR-106b-5p;hsa-miR-141-3p;hsa-miR-17-5p;hsa-miR-182-5p;hsa-miR-186-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-320b;hsa-miR-590-3p | 10 | CCND2 | Sponge network | -1.826 | 3.0E-5 | -1.641 | 0 | 0.36 |
| 9 | RP11-284N8.3 |
hsa-miR-106b-5p;hsa-miR-141-3p;hsa-miR-17-5p;hsa-miR-182-5p;hsa-miR-185-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-320b;hsa-miR-590-3p;hsa-miR-96-5p | 11 | CCND2 | Sponge network | -0.761 | 0.05061 | -1.641 | 0 | 0.36 |
| 10 | CTD-2013N24.2 |
hsa-miR-106b-5p;hsa-miR-141-3p;hsa-miR-15a-5p;hsa-miR-16-5p;hsa-miR-17-5p;hsa-miR-182-5p;hsa-miR-185-5p;hsa-miR-186-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-501-5p;hsa-miR-590-3p | 13 | CCND2 | Sponge network | -1.745 | 0 | -1.641 | 0 | 0.354 |
| 11 | AC109642.1 |
hsa-miR-106b-5p;hsa-miR-141-3p;hsa-miR-15a-5p;hsa-miR-16-5p;hsa-miR-17-5p;hsa-miR-182-5p;hsa-miR-185-5p;hsa-miR-186-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-320b;hsa-miR-590-3p;hsa-miR-96-5p | 14 | CCND2 | Sponge network | -2.791 | 0 | -1.641 | 0 | 0.339 |
| 12 | GAS6-AS2 |
hsa-miR-106b-5p;hsa-miR-141-3p;hsa-miR-15a-5p;hsa-miR-16-5p;hsa-miR-17-5p;hsa-miR-182-5p;hsa-miR-185-5p;hsa-miR-186-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p | 11 | CCND2 | Sponge network | -1.761 | 0 | -1.641 | 0 | 0.337 |
| 13 | RP11-354E11.2 |
hsa-miR-106b-5p;hsa-miR-16-5p;hsa-miR-17-5p;hsa-miR-182-5p;hsa-miR-185-5p;hsa-miR-186-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-590-3p;hsa-miR-96-5p | 11 | CCND2 | Sponge network | -2.138 | 0 | -1.641 | 0 | 0.335 |
| 14 | RP11-1024P17.1 |
hsa-miR-106b-5p;hsa-miR-130b-3p;hsa-miR-141-3p;hsa-miR-148b-3p;hsa-miR-17-5p;hsa-miR-186-5p;hsa-miR-18a-5p;hsa-miR-193a-3p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-25-3p;hsa-miR-301a-3p | 13 | PTEN | Sponge network | -2.062 | 0 | -0.419 | 0.00014 | 0.325 |
| 15 | RP11-166D19.1 |
hsa-miR-106b-5p;hsa-miR-141-3p;hsa-miR-17-5p;hsa-miR-182-5p;hsa-miR-185-5p;hsa-miR-186-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-320b;hsa-miR-96-5p | 11 | CCND2 | Sponge network | -0.582 | 0.05253 | -1.641 | 0 | 0.322 |
| 16 | LINC00702 |
hsa-miR-103a-3p;hsa-miR-106b-5p;hsa-miR-130b-3p;hsa-miR-141-3p;hsa-miR-148b-3p;hsa-miR-17-5p;hsa-miR-186-5p;hsa-miR-18a-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-25-3p;hsa-miR-301a-3p;hsa-miR-454-3p;hsa-miR-92a-3p;hsa-miR-93-5p | 16 | PTEN | Sponge network | -2.856 | 0 | -0.419 | 0.00014 | 0.312 |
| 17 | RP11-389C8.2 |
hsa-miR-103a-3p;hsa-miR-106b-5p;hsa-miR-130b-3p;hsa-miR-141-3p;hsa-miR-148b-3p;hsa-miR-17-5p;hsa-miR-186-5p;hsa-miR-18a-5p;hsa-miR-193a-3p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-301a-3p;hsa-miR-93-5p | 14 | PTEN | Sponge network | -2.039 | 0 | -0.419 | 0.00014 | 0.303 |
| 18 | FENDRR |
hsa-miR-106b-5p;hsa-miR-141-3p;hsa-miR-16-5p;hsa-miR-17-5p;hsa-miR-182-5p;hsa-miR-185-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-320b;hsa-miR-450b-5p;hsa-miR-590-3p;hsa-miR-96-5p | 13 | CCND2 | Sponge network | -4.222 | 0 | -1.641 | 0 | 0.301 |
| 19 | RP11-378A13.1 |
hsa-miR-106b-5p;hsa-miR-141-3p;hsa-miR-15a-5p;hsa-miR-17-5p;hsa-miR-182-5p;hsa-miR-185-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-590-3p | 10 | CCND2 | Sponge network | -1.713 | 0 | -1.641 | 0 | 0.301 |
| 20 | BAIAP2-AS1 |
hsa-miR-106a-5p;hsa-miR-106b-5p;hsa-miR-16-5p;hsa-miR-17-5p;hsa-miR-193a-3p;hsa-miR-193b-3p;hsa-miR-20a-5p;hsa-miR-20b-5p;hsa-miR-365a-3p;hsa-miR-93-5p | 10 | CCND1 | Sponge network | -0.182 | 0.51705 | -0.296 | 0.2554 | 0.3 |
| 21 | LINC00922 |
hsa-miR-106b-5p;hsa-miR-141-3p;hsa-miR-16-5p;hsa-miR-17-5p;hsa-miR-185-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-320b;hsa-miR-501-5p | 10 | CCND2 | Sponge network | -0.842 | 0.11239 | -1.641 | 0 | 0.298 |
| 22 | RP11-166D19.1 |
hsa-miR-103a-3p;hsa-miR-106b-5p;hsa-miR-130b-3p;hsa-miR-141-3p;hsa-miR-148b-3p;hsa-miR-17-5p;hsa-miR-186-5p;hsa-miR-18a-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-25-3p;hsa-miR-301a-3p;hsa-miR-454-3p;hsa-miR-92a-3p | 15 | PTEN | Sponge network | -0.582 | 0.05253 | -0.419 | 0.00014 | 0.295 |
| 23 | RP11-416I2.1 |
hsa-miR-106a-5p;hsa-miR-106b-5p;hsa-miR-15b-5p;hsa-miR-16-5p;hsa-miR-17-5p;hsa-miR-193a-3p;hsa-miR-19a-3p;hsa-miR-19b-1-5p;hsa-miR-20a-5p;hsa-miR-20b-5p;hsa-miR-93-5p | 11 | CCND1 | Sponge network | 3.177 | 1.0E-5 | -0.296 | 0.2554 | 0.294 |
| 24 | RP11-456K23.1 |
hsa-miR-106b-5p;hsa-miR-141-3p;hsa-miR-15a-5p;hsa-miR-16-5p;hsa-miR-17-5p;hsa-miR-182-5p;hsa-miR-185-5p;hsa-miR-186-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-450b-5p;hsa-miR-501-5p;hsa-miR-590-3p | 14 | CCND2 | Sponge network | -1.488 | 0 | -1.641 | 0 | 0.292 |
| 25 | WDFY3-AS2 |
hsa-miR-106b-5p;hsa-miR-130b-3p;hsa-miR-141-3p;hsa-miR-148b-3p;hsa-miR-17-5p;hsa-miR-18a-5p;hsa-miR-193a-3p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-25-3p;hsa-miR-301a-3p | 12 | PTEN | Sponge network | -1.297 | 0 | -0.419 | 0.00014 | 0.292 |
| 26 | TBX5-AS1 |
hsa-miR-103a-3p;hsa-miR-106b-5p;hsa-miR-130b-3p;hsa-miR-141-3p;hsa-miR-148b-3p;hsa-miR-17-5p;hsa-miR-186-5p;hsa-miR-18a-5p;hsa-miR-193a-3p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-25-3p;hsa-miR-301a-3p;hsa-miR-92a-3p | 15 | PTEN | Sponge network | -2.108 | 0 | -0.419 | 0.00014 | 0.286 |
| 27 | MIR497HG |
hsa-miR-106b-5p;hsa-miR-141-3p;hsa-miR-15a-5p;hsa-miR-16-5p;hsa-miR-17-5p;hsa-miR-182-5p;hsa-miR-185-5p;hsa-miR-186-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-450b-5p;hsa-miR-501-5p;hsa-miR-96-5p | 14 | CCND2 | Sponge network | -2.142 | 0 | -1.641 | 0 | 0.271 |
| 28 | DNM3OS |
hsa-miR-106b-5p;hsa-miR-141-3p;hsa-miR-16-5p;hsa-miR-17-5p;hsa-miR-182-5p;hsa-miR-185-5p;hsa-miR-186-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-320b;hsa-miR-501-5p;hsa-miR-590-3p | 13 | CCND2 | Sponge network | 0.053 | 0.85755 | -1.641 | 0 | 0.27 |
| 29 | MAGI2-AS3 |
hsa-miR-103a-3p;hsa-miR-106b-5p;hsa-miR-130b-3p;hsa-miR-141-3p;hsa-miR-148b-3p;hsa-miR-17-5p;hsa-miR-186-5p;hsa-miR-18a-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-25-3p;hsa-miR-301a-3p;hsa-miR-454-3p;hsa-miR-92a-3p;hsa-miR-93-5p | 16 | PTEN | Sponge network | -1.892 | 0 | -0.419 | 0.00014 | 0.268 |
| 30 | RP11-399O19.9 | hsa-miR-106b-5p;hsa-miR-130b-3p;hsa-miR-17-5p;hsa-miR-186-5p;hsa-miR-18a-5p;hsa-miR-19a-3p;hsa-miR-19b-3p;hsa-miR-20a-5p;hsa-miR-25-3p;hsa-miR-301a-3p;hsa-miR-93-5p | 11 | PTEN | Sponge network | -0.873 | 0.00072 | -0.419 | 0.00014 | 0.264 |
| 31 | AC003991.3 |
hsa-miR-106a-5p;hsa-miR-106b-5p;hsa-miR-16-1-3p;hsa-miR-16-5p;hsa-miR-17-5p;hsa-miR-193a-3p;hsa-miR-193b-3p;hsa-miR-19a-3p;hsa-miR-19b-1-5p;hsa-miR-20a-5p;hsa-miR-20b-5p;hsa-miR-365a-3p;hsa-miR-93-5p | 13 | CCND1 | Sponge network | -0.787 | 0.08132 | -0.296 | 0.2554 | 0.255 |
| 32 | LIPE-AS1 | hsa-miR-103a-3p;hsa-miR-106b-5p;hsa-miR-130b-3p;hsa-miR-17-5p;hsa-miR-186-5p;hsa-miR-18a-5p;hsa-miR-193a-3p;hsa-miR-19a-3p;hsa-miR-20a-5p;hsa-miR-301a-3p;hsa-miR-93-5p | 11 | PTEN | Sponge network | -0.734 | 0.00039 | -0.419 | 0.00014 | 0.254 |