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-34a-5p | BCL2 | 0.13 | 0.13326 | -0.9 | 0 | miRTarBase | -0.22 | 0.00143 | 24565525; 22623155; 21399894; 23155233; 24444609; 20687223; 24988056; 18803879; 19714243; 25053345; 20433755; 22964582; 23862748 | In vitro and in vivo experiments showed that miR-34a and DOX can be efficiently encapsulated into HA-CS NPs and delivered into tumor cells or tumor tissues and enhance anti-tumor effects of DOX by suppressing the expression of non-pump resistance and anti-apoptosis proto-oncogene Bcl-2;MiR 34a inhibits proliferation and migration of breast cancer through down regulation of Bcl 2 and SIRT1; In this study we aimed to determine the effect of miR-34a on the growth of breast cancer and to investigate whether its effect is achieved by targeting Bcl-2 and SIRT1; Bcl-2 and SIRT1 as the targets of miR-34a were found to be in reverse correlation with ectopic expression of miR-34a;Quantitative PCR and western analysis confirmed decreased expression of two genes BCL-2 and CCND1 in docetaxel-resistant cells which are both targeted by miR-34a;The miR-34a expression levels in cells after irradiation at 30 and 60 Gy were 0.17- and 18.7-times the BCL2 and caspase-9 expression levels respectively;Functional analyses further indicate that restoration of miR-34a inhibits B cell lymphoma-2 Bcl-2 protein expression to withdraw the survival advantage of these resistant NSCLC cells;Thus in PC3PR cells reduced expression of miR-34a confers paclitaxel resistance via up-regulating SIRT1 and Bcl2 expression; MiR-34a and its downstream targets SIRT1 and Bcl2 play important roles in the development of paclitaxel resistance all of which can be useful biomarkers and promising therapeutic targets for the drug resistance in hormone-refractory prostate cancer;Target analysis indicated that micro RNA miR-34a directly regulates Bcl-2 and miR-34a overexpression decreased Bcl-2 protein level in gastric cancer cells; We also found that luteolin upregulates miR-34a expression and downregulates Bcl-2 expression; Based on these results we can draw the conclusion that luteolin partly decreases Bcl-2 expression through upregulating miR-34a expression;miR-34 targets Notch HMGA2 and Bcl-2 genes involved in the self-renewal and survival of cancer stem cells; Human gastric cancer cells were transfected with miR-34 mimics or infected with the lentiviral miR-34-MIF expression system and validated by miR-34 reporter assay using Bcl-2 3'UTR reporter; Human gastric cancer Kato III cells with miR-34 restoration reduced the expression of target genes Bcl-2 Notch and HMGA2; Bcl-2 3'UTR reporter assay showed that the transfected miR-34s were functional and confirmed that Bcl-2 is a direct target of miR-34; The mechanism of miR-34-mediated suppression of self-renewal appears to be related to the direct modulation of downstream targets Bcl-2 Notch and HMGA2 indicating that miR-34 may be involved in gastric cancer stem cell self-renewal/differentiation decision-making;Among the target proteins regulated by miR-34 are Notch pathway proteins and Bcl-2 suggesting the possibility of a role for miR-34 in the maintenance and survival of cancer stem cells; Our data support the view that miR-34 may be involved in pancreatic cancer stem cell self-renewal potentially via the direct modulation of downstream targets Bcl-2 and Notch implying that miR-34 may play an important role in pancreatic cancer stem cell self-renewal and/or cell fate determination;Manipulating miR-34a in prostate cancer cells confirms that this miRNA regulates BCL-2 and may in part regulate response to docetaxel;For instance miR-34a up-regulation corresponded with a down-regulation of BCL2 protein; Treating Par-4-overexpressing HT29 cells with a miR-34a antagomir functionally reversed both BCL2 down-regulation and apoptosis by 5-FU;Tumors harvested from these lungs have elevated levels of oncogenic miRNAs miR-21 and miR-155; are deficient for p53-regulated miRNAs; and have heightened expression of miR-34 target genes such as Met and Bcl-2;MicroRNA 34a targets Bcl 2 and sensitizes human hepatocellular carcinoma cells to sorafenib treatment; HCC tissues with lower miR-34a expression displayed higher expression of Bcl-2 protein than those with high expression of miR-34a; therefore an inverse correlation is evident between the miR-34a level and Bcl-2 expression; Bioinformatics and luciferase reporter assays revealed that miR-34a binds the 3'-UTR of the Bcl-2 mRNA and represses its translation; Western blotting analysis and qRT-PCR confirmed that Bcl-2 is inhibited by miR-34a overexpression; Functional analyses indicated that the restoration of miR-34a reduced cell viability promoted cell apoptosis and potentiated sorafenib-induced apoptosis and toxicity in HCC cell lines by inhibiting Bcl-2 expression |
| 2 | hsa-miR-34a-5p | DLL1 | 0.13 | 0.13326 | -0.95 | 0 | miRTarBase | -0.18 | 0.0003 | 22438124 | Delta tocotrienol suppresses Notch 1 pathway by upregulating miR 34a in nonsmall cell lung cancer cells |
| 3 | hsa-miR-152-3p | DNMT1 | -0.27 | 0.00639 | 1.04 | 0 | miRTarBase | -0.16 | 0 | 27475839; 21868754; 25004396; 20578129; 24998573; 23318422 | mRNA and protein expression profile of DNMT1 implicate that miR-152 targets DNMT1 mRNA and inhibits its protein expression; Further experiments revealed that DNMT1 plays crucial role for regulation of miR-152 gene; When DNMT1 protein function is blocked miR-152 expression prevails and destroys the mRNA of DNMT1; this molecular regulatory mechanism is creating a cyclic feedback loop which is now focused as DNMT1/miR-152 switch for on/off of DNMT1 target genes; We have demonstrated further that DNMT1 down regulation mediated upregulation of CDH1 hereafter DNMT1/CDH1 loop in presence of ectopic-excess of miR-152 prevents migration of cancer cells;Epigenetic silencing documented in miR-152 was consistent with its location at 17q21.32 in intron 1 of the COPZ2 gene which is also silenced often in endometrial cancer by DNA hypermethylation and also with evidence that miR-152 targets the DNA methyltransferase DNMT1;There appeared to be a reciprocal regulatory relationship of miR-152/DNMT1 expression as cells treated with siRNA DNMT1 caused miR-152 to be re-expressed in all cell lines;Our results showed that the expression of microRNA-152 miR-152 was frequently down-regulated in HBV-related HCC tissues in comparison with adjacent noncancerous hepatic tissues and was inversely correlated to DNA methyltransferase 1 DNMT1 messenger RNA mRNA expression in HBV-related HCCs; The forced expression of miR-152 in liver cell lines resulted in a marked reduction of the expression of DNMT1 at both the mRNA and protein levels by directly targeting the 3' untranslated regions of DNMT1; Our findings suggest that miR-152 is frequently down-regulated and regulates DNMT1 in HBV-related HCC;Furthermore Western blotting showed that the miR-152 mimic downregulated Wnt-1 DNMT1 ERK1/2 AKT and TNFRS6B signaling;MiR 152 and miR 185 co contribute to ovarian cancer cells cisplatin sensitivity by targeting DNMT1 directly: a novel epigenetic therapy independent of decitabine; The overexpression of miR-152 or miR-185 increased cisplatin sensitivity of SKOV3/DDP and A2780/DDP cells by inhibiting proliferation and promoting apoptosis then we further confirmed that these miRNAs functioned through suppressing DNA methyltransferase 1 DNMT1 directly; Our results indicated that miR-152 and miR-185 were involved in ovarian cancer cisplatin resistance in vitro and in vivo by targeting DNMT1 directly |
| 4 | hsa-miR-140-5p | DNPEP | -0.76 | 0 | 0.47 | 0 | miRTarBase | -0.16 | 0 | NA | |
| 5 | hsa-miR-194-5p | HBEGF | 0.47 | 0 | -1.07 | 0 | miRTarBase | -0.13 | 0.00361 | NA | |
| 6 | hsa-miR-152-3p | HLA-G | -0.27 | 0.00639 | 0.48 | 0.01437 | miRTarBase | -0.19 | 0.00481 | 26187665; 26627200 | Long non coding RNA HOTAIR promotes HLA G expression via inhibiting miR 152 in gastric cancer cells; On the other hand bioinformatics analysis indicated the interaction between HOTAIR and miR-152 which shows potential regulation on HLA-G; Therefore it was concluded that HOTAIR overexpression might also get involved in tumor escape mechanisms involving HLA-G upregulation via inhibiting miR-152;TGF β induces HLA G expression through inhibiting miR 152 in gastric cancer cells; This study aims to verify the correlations between HLA-G and TGF-β involving the potential targeting of miR-152 on HLA-G; Furthermore miR-152 expression could be inhibited by TGF-β and the negative post-transcriptionally regulation of miR-152 on HLA-G was also demonstrated through gain- and loss-of-function studies; Besides miR-152 overexpression repressed HLA-G up-regulation induced by TGF-β; And miR-152 expression levels showed inversely proportional to both HLA-G and also TGF-β levels in GC patients; TGF-β could induce HLA-G expression in GC by inhibiting miR-152 involving its negative regulation on HLA-G; Since TGF-β induced HLA-G up-regulation plays important role in immune escape a potential application of miR-152 was suggested in GC treatment or miR-152 might be one potential biomarker for GC |
| 7 | hsa-miR-194-5p | ITGA9 | 0.47 | 0 | -1.81 | 0 | miRTarBase | -0.12 | 0.04781 | NA | |
| 8 | hsa-miR-34a-5p | JAG1 | 0.13 | 0.13326 | -0.64 | 0 | miRTarBase | -0.11 | 0.00421 | NA | |
| 9 | hsa-miR-34a-5p | KLB | 0.13 | 0.13326 | -4.4 | 0 | miRTarBase | -0.23 | 0.01748 | NA | |
| 10 | hsa-miR-34a-5p | MET | 0.13 | 0.13326 | -2.37 | 0 | miRTarBase | -0.26 | 0.00075 | 23243217; 26104764; 22457788; 23593387; 19006648; 19773441; 19029026 | Detection of miR 34a promoter methylation in combination with elevated expression of c Met and β catenin predicts distant metastasis of colon cancer; Using a case-control study design of 94 primary colon cancer samples with and without liver metastases we determined CpG methylation frequencies of miR-34a and miR-34b/c promoters expression of miR-34a and its targets c-Met Snail and β-catenin and their prognostic value; Decreased miR-34a expression was associated with upregulation of c-Met Snail and β-catenin protein levels P = 0.031 0.132 and 0.004 which were associated with distant metastases P = 0.001 0.017 and 0.005; In a confounder-adjusted multivariate regression model miR-34a methylation high c-Met and β-catenin levels provided the most significant prognostic information about metastases to the liver P = 0.014 0.031 and 0.058 and matched pairs showed a higher prevalence of these risk factors in the samples with distant spread P = 0.029; Silencing of miR-34a and upregulation of c-Met Snail and β-catenin expression is associated with liver metastases of colon cancer; Detection of miR-34a silencing in resected primary colon cancer may be of prognostic value especially in combination with detection of c-Met and β-catenin expression;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;c-Met is a target of miR-34a and regulates the migration and invasion of osteosarcoma cells; Osteosarcoma cells over-expressing miR-34a exhibited a significant decrease in the expression levels of c-Met mRNA and protein simultaneously; The results presented in this study demonstrated that over-expression of miR-34a could inhibit the tumor growth and metastasis of osteosarcoma probably through down regulating c-Met; And there are other putative miR-34a target genes beside c-Met which could potentially be key players in the development of osteosarcoma;Underexpression of miR 34a in hepatocellular carcinoma and its contribution towards enhancement of proliferating inhibitory effects of agents targeting c MET; In addition miR-34a mimic enhanced the effect of cell proliferation inhibition and caspase activity induction of agents targeting c-MET siRNAs and small molecular inhibitor su11274;miR 34a inhibits migration and invasion by down regulation of c Met expression in human hepatocellular carcinoma cells; miR-34a directly targeted c-Met and reduced both mRNA and protein levels of c-Met; thus decreased c-Met-induced phosphorylation of extracellular signal-regulated kinases 1 and 2 ERK1/2; Taken together these results provide evidence to show the suppression role of miR-34a in tumor migration and invasion through modulation of the c-Met signaling pathway;miR-34a levels in human gliomas inversely correlated to c-Met levels measured in the same tumors; Forced expression of c-Met or Notch-1/Notch-2 transcripts lacking the 3'-untranslated region sequences partially reversed the effects of miR-34a on cell cycle arrest and cell death in glioma cells and stem cells respectively; They show that miR-34a suppresses brain tumor growth by targeting c-Met and Notch;MicroRNA 34a inhibits uveal melanoma cell proliferation and migration through downregulation of c Met; In addition expression of c-Met and cell cycle-related proteins was determined by Western blotting and immunofluorescence after the introduction of miR-34a miR-34a is actively expressed in melanocytes but not in uveal melanoma cells based on Northern blot analysis; After identification of two putative miR-34a binding sites within the 3' UTR of the human c-Met mRNA miR-34a was shown to suppress luciferase activity using HEK293 cells with a luciferase reporter construct containing the binding sites; miR-34a was confirmed to downregulate the expression of c-Met protein by Western blotting and immunofluorescence; These results demonstrate that miR-34a acts as a tumor suppressor in uveal melanoma cell proliferation and migration through the downregulation of c-Met |
| 11 | hsa-miR-34a-5p | MYC | 0.13 | 0.13326 | -1.13 | 0 | miRTarBase | -0.22 | 0.00013 | 25572695; 25686834; 21460242; 22159222; 23640973; 22830357; 22235332 | The c-Myc and CD44 were confirmed as direct targets of miR-34a in EJ cell apoptosis induced by PRE;miR 34a induces cellular senescence via modulation of telomerase activity in human hepatocellular carcinoma by targeting FoxM1/c Myc pathway;Myc mediated repression of microRNA 34a promotes high grade transformation of B cell lymphoma by dysregulation of FoxP1;MicroRNA 34a suppresses malignant transformation by targeting c Myc transcriptional complexes in human renal cell carcinoma; We investigated the functional effects of microRNA-34a miR-34a on c-Myc transcriptional complexes in renal cell carcinoma; miR-34a down-regulated expression of multiple oncogenes including c-Myc by targeting its 3' untranslated region which was revealed by luciferase reporter assays; Our results demonstrate that miR-34a suppresses assembly and function of the c-Myc complex that activates or elongates transcription indicating a novel role of miR-34a in the regulation of transcription by c-Myc;Among them miR-34a was also associated with poor prognosis in 2 independent series of leukemic and nodal MCL and in cooperation with high expression of the MYC oncogene;We report that miR-34a did not inhibit cell proliferation notwithstanding a marked down-regulation of c-MYC;MicroRNA 34a modulates c Myc transcriptional complexes to suppress malignancy in human prostate cancer cells; We studied the functional effects of miR-34a on c-Myc transcriptional complexes in PC-3 prostate cancer cells; miR-34a downregulated expression of c-Myc oncogene by targeting its 3' UTR as shown by luciferase reporter assays; This is the first report to document that miR-34a suppresses assembly and function of the c-Myc-Skp2-Miz1 complex that activates RhoA and the c-Myc-pTEFB complex that elongates transcription of various genes suggesting a novel role of miR-34a in the regulation of transcription by c-Myc complex |
| 12 | hsa-miR-34a-5p | PDGFRA | 0.13 | 0.13326 | -1.84 | 0 | miRTarBase | -0.26 | 9.0E-5 | 22750848 | Mechanistically in addition to its direct regulation of platelet-derived growth factor receptor-alpha PDGFRA promoter enrichment analysis of context likelihood of relatedness-inferred mRNA nodes established miR-34a as a novel regulator of a SMAD4 transcriptional network |
| 13 | hsa-miR-194-5p | PTPN13 | 0.47 | 0 | -0.81 | 0 | miRTarBase | -0.21 | 0.00033 | NA | |
| 14 | hsa-miR-34a-5p | SIRT1 | 0.13 | 0.13326 | -0.6 | 0 | miRTarBase | -0.12 | 3.0E-5 | 22623155; 25826085; 25982144; 21067862; 20687223; 23954321; 26722316; 27126903; 26518892; 18834855 | MiR 34a inhibits proliferation and migration of breast cancer through down regulation of Bcl 2 and SIRT1; In this study we aimed to determine the effect of miR-34a on the growth of breast cancer and to investigate whether its effect is achieved by targeting Bcl-2 and SIRT1; Bcl-2 and SIRT1 as the targets of miR-34a were found to be in reverse correlation with ectopic expression of miR-34a;Dysregulation of the miR 34a SIRT1 axis inhibits breast cancer stemness; Sirtuin-1 SIRT1 is a direct target of miR-34a; Here we found low levels of miR-34a and high levels of SIRT1 in CD44+/CD24- breast cancer stem cells BCSCs; MiR-34a overexpression and knockdown of SIRT1 decreased proportion of BSCSs and mammosphere formation; In nude mice xenografts stable expression of miR-34a and silencing of SIRT1 reduced tumor burden; Taken together our results demonstrated that miR-34a inhibits proliferative potential of BCSCs in vitro and in vivo at least partially by downregulating SIRT1;5 Aminolevulinic acid mediated sonodynamic therapy induces anti tumor effects in malignant melanoma via p53 miR 34a Sirt1 axis; Therefore the p53 miR-34a and SIRT1 constituted a positive feedback loop;Sirt1 which is one of the target genes for miR-34a and related to drug-resistance was strikingly up-regulated in the 5-FU-resistant cells; The ectopic expression of miR-34a in the 5-FU-resistant cells inhibited growth as in the parental cells and attenuated the resistance to 5-FU through the down-regulation of Sirt1 and E2F3; These findings suggest that miR-34a targeting the Sirt1 and E2F3 genes could negatively regulate at least in part the resistance to 5-FU in human colorectal cancer DLD-1 cells;We aimed to elucidate the molecular mechanisms underlying paclitaxel resistance of hormone-refractory prostate cancer with a special focus on the roles of miR-34a and SIRT1; MiR-34a over-expression and SIRT1 knockdown attenuated paclitaxel resistance of PC3PR cells; Thus in PC3PR cells reduced expression of miR-34a confers paclitaxel resistance via up-regulating SIRT1 and Bcl2 expression; MiR-34a and its downstream targets SIRT1 and Bcl2 play important roles in the development of paclitaxel resistance all of which can be useful biomarkers and promising therapeutic targets for the drug resistance in hormone-refractory prostate cancer;Interestingly RES increased the intracellular expression level of miR-34a which down-regulated the target gene E2F3 and its downstream Sirt1 resulting in growth inhibition;miR 34a inhibits cell proliferation in prostate cancer by downregulation of SIRT1 expression; The role of miR-34a in regulating sirtuin 1 SIRT1 in prostate cancer remains unclear; The objective of the present study was to investigate the biological function and molecular mechanisms of miR-34a regulation of SIRT1 in human prostate cancer samples and the human prostate cancer cell line PC-3; Fresh prostate tissues were obtained from patients and the miR-34a expression in prostate cancer tissues was measured using reverse transcription-quantitative polymerase chain reaction RT-qPCR qPCR and western blotting were performed to assess the effects of miR-34a overexpression on SIRT1 regulation in PC-3 cells and the cell growth was assessed by Cell Counting Kit-8 CCK-8; SIRT1 expression levels in PC-3 cells with over-expression of miR-34a were significantly reduced compared with those in the negative control P<0.05; In conclusion miR-34a inhibits the human prostate cancer cell proliferation in part through the downregulation of SIRT1 expression;In addition the present micellar system facilitated the escape of miR-34a from the endosome and release of DOX into the cell nucleus leading to the downregulation of silent information regulator 1 SIRT1 expression and inhibition of DU145 and PC3 androgen-independent prostate cancer cell proliferation;For example overexpressing miR-34a a master regulator of tumor suppression attenuates chemoresistance to 5-FU by downregulating silent information regulator 1 SIRT1 and E2F3;In PC3 cell ectopic expression of miR-34a decreased the SIRT1 mRNA and protein levels as well as protein levels of known direct target genes; Reporter assays revealed that miR-34a-induced SIRT1 inhibition occurred at the transcriptional but not post-transcriptional level despite the presence of a potential miR-34a binding site within its 3'-UTR |
| 15 | hsa-miR-194-5p | SOCS2 | 0.47 | 0 | -1.86 | 0 | miRTarBase | -0.27 | 0.0001 | 22102710 | Functional studies indicated that CDKN1A/p21 and SOCS2 expression is directly regulated by miR-20a/-20b and miR-194 respectively; miR-20a/b and miR-194 target CDKN1A and SOCS2 in follicular lymphoma potentially contributing to tumor cell proliferation and survival |
| 16 | hsa-miR-140-5p | SOX2 | -0.76 | 0 | 1.63 | 0 | miRTarBase | -0.26 | 0.02297 | 23060440; 25426255 | We found that the stem cell self-renewal regulator SOX2 is a novel target of miR-140 and that this miR-140/SOX2 pathway critically regulates breast tumor-initiating cell survival providing a new link between ERα signaling and breast cancer stem cell maintenance;miR-140 plays an important tumor suppressive role in the Wnt SOX2 and SOX9 stem cell regulator pathways |
| 17 | hsa-miR-34a-5p | SOX2 | 0.13 | 0.13326 | 1.63 | 0 | miRTarBase | -0.28 | 0.04379 | NA | |
| 18 | hsa-miR-194-5p | SOX5 | 0.47 | 0 | -2.72 | 0 | miRTarBase | -0.21 | 0.01499 | NA | |
| 19 | hsa-miR-34a-5p | SYT1 | 0.13 | 0.13326 | 0.52 | 0.08931 | miRTarBase | -0.25 | 0.04318 | NA | |
| 20 | hsa-miR-194-5p | TLN2 | 0.47 | 0 | -1.84 | 0 | miRTarBase | -0.2 | 0 | NA |
| Num | GO | Overlap | Size | P Value | Adj. P Value |
|---|---|---|---|---|---|
| 1 | REGULATION OF CELL PROLIFERATION | 11 | 1496 | 1.706e-08 | 7.937e-05 |
| 2 | NEPHRON DEVELOPMENT | 5 | 115 | 6.279e-08 | 0.0001461 |
| 3 | REGULATION OF PHOSPHATIDYLINOSITOL 3 KINASE SIGNALING | 5 | 138 | 1.565e-07 | 0.000182 |
| 4 | POSITIVE REGULATION OF MULTICELLULAR ORGANISMAL PROCESS | 10 | 1395 | 1.362e-07 | 0.000182 |
| 5 | POSITIVE REGULATION OF RESPONSE TO STIMULUS | 11 | 1929 | 2.374e-07 | 0.0001987 |
| 6 | REGULATION OF CELL DIFFERENTIATION | 10 | 1492 | 2.563e-07 | 0.0001987 |
| 7 | POSITIVE REGULATION OF CELL COMMUNICATION | 10 | 1532 | 3.284e-07 | 0.0001996 |
| 8 | POSITIVE REGULATION OF DEVELOPMENTAL PROCESS | 9 | 1142 | 3.432e-07 | 0.0001996 |
| 9 | NEURONAL STEM CELL POPULATION MAINTENANCE | 3 | 19 | 6.976e-07 | 0.0003607 |
| 10 | RENAL TUBULE DEVELOPMENT | 4 | 78 | 7.935e-07 | 0.0003634 |
| 11 | NEGATIVE REGULATION OF CELL DIFFERENTIATION | 7 | 609 | 8.591e-07 | 0.0003634 |
| 12 | MORPHOGENESIS OF AN EPITHELIUM | 6 | 400 | 1.342e-06 | 0.0005202 |
| 13 | NEPHRON EPITHELIUM DEVELOPMENT | 4 | 93 | 1.61e-06 | 0.0005761 |
| 14 | CELL FATE COMMITMENT | 5 | 227 | 1.841e-06 | 0.0006118 |
| 15 | RESPONSE TO GROWTH FACTOR | 6 | 475 | 3.628e-06 | 0.001125 |
| 16 | KIDNEY EPITHELIUM DEVELOPMENT | 4 | 125 | 5.241e-06 | 0.001456 |
| 17 | NEGATIVE REGULATION OF DEVELOPMENTAL PROCESS | 7 | 801 | 5.319e-06 | 0.001456 |
| 18 | POSITIVE REGULATION OF CELL PROLIFERATION | 7 | 814 | 5.914e-06 | 0.001529 |
| 19 | TISSUE MORPHOGENESIS | 6 | 533 | 7.032e-06 | 0.001645 |
| 20 | UROGENITAL SYSTEM DEVELOPMENT | 5 | 299 | 7.072e-06 | 0.001645 |
| 21 | REGULATION OF INTRACELLULAR SIGNAL TRANSDUCTION | 9 | 1656 | 7.688e-06 | 0.001703 |
| 22 | REGULATION OF MULTICELLULAR ORGANISMAL DEVELOPMENT | 9 | 1672 | 8.32e-06 | 0.001738 |
| 23 | TUBE DEVELOPMENT | 6 | 552 | 8.592e-06 | 0.001738 |
| 24 | RESPONSE TO IONIZING RADIATION | 4 | 145 | 9.439e-06 | 0.00183 |
| 25 | TUBE MORPHOGENESIS | 5 | 323 | 1.028e-05 | 0.001914 |
| 26 | GLOMERULUS DEVELOPMENT | 3 | 49 | 1.303e-05 | 0.002331 |
| 27 | NEGATIVE REGULATION OF RESPONSE TO STIMULUS | 8 | 1360 | 1.719e-05 | 0.002962 |
| 28 | REGULATION OF GROWTH | 6 | 633 | 1.872e-05 | 0.003112 |
| 29 | NEGATIVE REGULATION OF MULTICELLULAR ORGANISMAL PROCESS | 7 | 983 | 2.03e-05 | 0.003257 |
| 30 | REGULATION OF CELL GROWTH | 5 | 391 | 2.582e-05 | 0.004005 |
| 31 | EAR DEVELOPMENT | 4 | 195 | 3.028e-05 | 0.004546 |
| 32 | TISSUE DEVELOPMENT | 8 | 1518 | 3.823e-05 | 0.00556 |
| 33 | ENDOTHELIAL CELL DIFFERENTIATION | 3 | 72 | 4.159e-05 | 0.005693 |
| 34 | MUSCLE STRUCTURE DEVELOPMENT | 5 | 432 | 4.16e-05 | 0.005693 |
| 35 | LOOP OF HENLE DEVELOPMENT | 2 | 11 | 4.679e-05 | 0.00622 |
| 36 | INTRACELLULAR SIGNAL TRANSDUCTION | 8 | 1572 | 4.92e-05 | 0.006359 |
| 37 | POSITIVE REGULATION OF GROWTH | 4 | 238 | 6.585e-05 | 0.008282 |
| 38 | OVULATION CYCLE PROCESS | 3 | 88 | 7.58e-05 | 0.009051 |
| 39 | ENDOTHELIUM DEVELOPMENT | 3 | 90 | 8.105e-05 | 0.009051 |
| 40 | SENSORY ORGAN DEVELOPMENT | 5 | 493 | 7.789e-05 | 0.009051 |
| 41 | TRANSMEMBRANE RECEPTOR PROTEIN TYROSINE KINASE SIGNALING PATHWAY | 5 | 498 | 8.17e-05 | 0.009051 |
| 42 | POSITIVE REGULATION OF CELL DIFFERENTIATION | 6 | 823 | 8.16e-05 | 0.009051 |
| 43 | REGULATION OF PROTEIN MODIFICATION PROCESS | 8 | 1710 | 8.989e-05 | 0.009727 |
| Num | GO | Overlap | Size | P Value | Adj. P Value |
|---|---|---|---|---|---|
| 1 | RECEPTOR BINDING | 10 | 1476 | 2.316e-07 | 0.0002152 |
| Num | GO | Overlap | Size | P Value | Adj. P Value |
|---|
Over-represented Pathway
| Num | Pathway | Pathview | Overlap | Size | P Value | Adj. P Value |
|---|---|---|---|---|---|---|
| 1 | Focal_adhesion_hsa04510 | 5 | 199 | 9.628e-07 | 5.007e-05 | |
| 2 | Jak_STAT_signaling_pathway_hsa04630 | 4 | 162 | 1.462e-05 | 0.00027 | |
| 3 | PI3K_Akt_signaling_pathway_hsa04151 | 5 | 352 | 1.558e-05 | 0.00027 | |
| 4 | Cellular_senescence_hsa04218 | 3 | 160 | 0.0004431 | 0.005761 | |
| 5 | Rap1_signaling_pathway_hsa04015 | 3 | 206 | 0.0009239 | 0.008144 | |
| 6 | Notch_signaling_pathway_hsa04330 | 2 | 48 | 0.0009397 | 0.008144 | |
| 7 | MAPK_signaling_pathway_hsa04010 | 3 | 295 | 0.002584 | 0.01893 | |
| 8 | ErbB_signaling_pathway_hsa04012 | 2 | 85 | 0.002912 | 0.01893 | |
| 9 | Apoptosis_hsa04210 | 2 | 138 | 0.007484 | 0.03892 | |
| 10 | Signaling_pathways_regulating_pluripotency_of_stem_cells_hsa04550 | 2 | 139 | 0.007589 | 0.03892 | |
| 11 | Cell_adhesion_molecules_.CAMs._hsa04514 | 2 | 145 | 0.008233 | 0.03892 | |
| 12 | Hippo_signaling_pathway_hsa04390 | 2 | 154 | 0.009244 | 0.04006 | |
| 13 | Regulation_of_actin_cytoskeleton_hsa04810 | 2 | 208 | 0.01639 | 0.06554 | |
| 14 | Ras_signaling_pathway_hsa04014 | 2 | 232 | 0.02012 | 0.07474 | |
| 15 | Endocytosis_hsa04144 | 2 | 244 | 0.02211 | 0.07665 | |
| 16 | Cytokine_cytokine_receptor_interaction_hsa04060 | 2 | 270 | 0.02669 | 0.08675 |
