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.
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-148a-3p | ACVR1 | -0.75 | 0 | -0.44 | 1.0E-5 | miRNAWalker2 validate; miRTarBase | -0.13 | 0.0001 | NA | |
2 | hsa-miR-192-5p | AFAP1L1 | -0.5 | 0.00345 | 0.54 | 1.0E-5 | miRNAWalker2 validate | -0.18 | 0 | NA | |
3 | hsa-miR-192-5p | AKAP7 | -0.5 | 0.00345 | -0.93 | 0 | miRNAWalker2 validate | -0.12 | 0.01301 | NA | |
4 | hsa-miR-27b-3p | ANKRD52 | -0.82 | 0 | 1.46 | 0 | miRNAWalker2 validate | -0.28 | 0 | NA | |
5 | hsa-miR-192-5p | ANLN | -0.5 | 0.00345 | 3.89 | 0 | miRNAWalker2 validate | -0.2 | 0.01824 | NA | |
6 | hsa-miR-192-5p | AP1S2 | -0.5 | 0.00345 | -0.4 | 0.00049 | miRNAWalker2 validate | -0.33 | 0 | NA | |
7 | hsa-miR-192-5p | AP3M2 | -0.5 | 0.00345 | 0.87 | 0 | miRNAWalker2 validate | -0.28 | 0 | NA | |
8 | hsa-miR-106b-5p | APC | 0.65 | 0 | -0.18 | 0.06792 | miRNAWalker2 validate; miRTarBase | -0.15 | 0.00024 | 23087084 | miR 106b downregulates adenomatous polyposis coli and promotes cell proliferation in human hepatocellular carcinoma; Moreover we demonstrated that miR-106b downregulates APC expression by directly targeting the 3'-untranslated region of APC messenger RNA; Taken together our results suggest that miR-106b plays an important role in promoting the proliferation of human hepatoma cells and presents a novel mechanism of micro RNA-mediated direct suppression of APC expression in cancer cells |
9 | hsa-miR-21-5p | APC | 1.51 | 0 | -0.18 | 0.06792 | miRNAWalker2 validate | -0.17 | 0 | 23773491; 24832083 | The prognostic significance of APC gene mutation and miR 21 expression in advanced stage colorectal cancer; The aim of this study was to analyse the association of APC gene mutation and miR-21 expression with clinical outcome in CRC patients; APC gene mutation and expression of APC and miR-21 were analysed by direct DNA sequencing and real-time reverse transcription polymerase chain reaction; APC gene expression was low in CRC and negatively correlated with miR-21 expression and gene mutation; In Taiwan downregulation of the APC gene in CRC correlated with gene mutation and miR-21 upregulation; APC mutation and miR-21 expression could be used to predict the clinical outcome of CRC especially in patients with advanced disease;MicroRNA 21 promotes tumour malignancy via increased nuclear translocation of β catenin and predicts poor outcome in APC mutated but not in APC wild type colorectal cancer; However in our preliminary data the prognostic value of miR-21 levels was observed only in adenomatous polyposis coli APC-mutated tumours not in APC-wild-type tumours; We enrolled 165 colorectal tumour to determine APC mutation miR-21 levels and nuclear β-catenin expression by direct sequencing real-time PCR and immunohistochemistry |
10 | hsa-miR-17-5p | ARHGAP5 | 0.7 | 2.0E-5 | -0.39 | 8.0E-5 | miRNAWalker2 validate | -0.17 | 0 | NA | |
11 | hsa-miR-192-5p | ARHGEF10 | -0.5 | 0.00345 | 0.05 | 0.78887 | miRNAWalker2 validate | -0.42 | 0 | NA | |
12 | hsa-miR-192-5p | ARL4C | -0.5 | 0.00345 | -0.83 | 1.0E-5 | miRNAWalker2 validate | -0.45 | 0 | NA | |
13 | hsa-miR-192-5p | ARNTL2 | -0.5 | 0.00345 | 0.02 | 0.94112 | miRNAWalker2 validate | -0.27 | 0.00197 | NA | |
14 | hsa-miR-192-5p | ASPH | -0.5 | 0.00345 | 0.47 | 0.00525 | miRNAWalker2 validate | -0.11 | 0.02603 | NA | |
15 | hsa-miR-20a-5p | ATL3 | 0.85 | 0 | 0.13 | 0.25255 | miRNAWalker2 validate | -0.2 | 0 | NA | |
16 | hsa-miR-192-5p | ATP10D | -0.5 | 0.00345 | -0.43 | 0.00646 | miRNAWalker2 validate | -0.13 | 0.00486 | NA | |
17 | hsa-miR-148a-3p | AURKB | -0.75 | 0 | 3.49 | 0 | miRNAWalker2 validate | -0.53 | 0 | NA | |
18 | hsa-miR-15b-5p | AXIN2 | 0.23 | 0.08248 | 0.11 | 0.75298 | miRTarBase | -0.45 | 0.00081 | NA | |
19 | hsa-miR-16-5p | AXIN2 | -0.4 | 0.0001 | 0.11 | 0.75298 | miRNAWalker2 validate; miRTarBase | -0.49 | 0.00421 | NA | |
20 | hsa-miR-192-5p | B3GALNT1 | -0.5 | 0.00345 | 0.61 | 0.001 | miRNAWalker2 validate | -0.42 | 0 | NA | |
21 | hsa-miR-192-5p | B3GNT5 | -0.5 | 0.00345 | 0.79 | 0.0009 | miRNAWalker2 validate | -0.18 | 0.00734 | NA | |
22 | hsa-miR-27b-3p | BAZ2A | -0.82 | 0 | 0.46 | 0 | miRNAWalker2 validate | -0.11 | 0.00278 | NA | |
23 | hsa-miR-192-5p | BBS7 | -0.5 | 0.00345 | 0.27 | 0.09013 | miRNAWalker2 validate | -0.17 | 0.00017 | NA | |
24 | hsa-miR-148a-3p | BCL2 | -0.75 | 0 | -0.35 | 0.02497 | miRNAWalker2 validate; miRTarBase | -0.31 | 0 | 21455217; 23975374 | MiR 148a promotes apoptosis by targeting Bcl 2 in colorectal cancer;MiR 148a regulates the growth and apoptosis in pancreatic cancer by targeting CCKBR and Bcl 2; Using western blot and luciferase activity assay CCKBR and Bcl-2 were identified as targets of miR-148a; Moreover we also found that the expression of Bcl-2 lacking in 3'UTR could abrogate the pro-apoptosis function of miR-148a |
25 | hsa-miR-192-5p | BCL2 | -0.5 | 0.00345 | -0.35 | 0.02497 | miRNAWalker2 validate | -0.34 | 0 | 26550150 | MicroRNA 192 regulates chemo resistance of lung adenocarcinoma for gemcitabine and cisplatin combined therapy by targeting Bcl 2; In this paper we try to test whether miR-192 regulates chemo-resistance in human carcinoma A549 mice model by targeting Bcl-2; MTT assay real-time RT-PCR western blotting assay were used to investigate miR-192 expression levels cell viability ratio and Bcl-2 protein expression levels; Bcl-2 mRNA and protein expression levels up-regulated in miR-192 inhibitor treated tumor; Bcl-2 is a key regulator for miR-192 related chemotherapy resistance; In this study we demonstrate that miR-192 regulates chemoresistance for gemcitabine and cisplatin combined chemotherapy in human adenocarcinoma lung cancer A549 cells and Bcl-2 is the target of miR-192 |
26 | hsa-miR-20a-5p | BCL2 | 0.85 | 0 | -0.35 | 0.02497 | miRNAWalker2 validate; miRTarBase | -0.31 | 0 | NA | |
27 | hsa-miR-192-5p | BICD1 | -0.5 | 0.00345 | 0.8 | 0.0004 | miRNAWalker2 validate | -0.46 | 0 | NA | |
28 | hsa-let-7b-5p | BIRC5 | -0.96 | 0 | 4.5 | 0 | miRNAWalker2 validate | -0.71 | 0 | NA | |
29 | hsa-miR-101-3p | BIRC5 | -1.48 | 0 | 4.5 | 0 | miRNAWalker2 validate | -1.33 | 0 | NA | |
30 | hsa-miR-10a-5p | BIRC5 | -1.48 | 0 | 4.5 | 0 | miRNAWalker2 validate | -0.71 | 0 | NA | |
31 | hsa-miR-203a-3p | BIRC5 | -1.34 | 9.0E-5 | 4.5 | 0 | miRTarBase | -0.13 | 0.00935 | 22713668; 27714672 | Luciferase assays were also performed to validate BIRC5 and LASP1 as miR-203 targets; Both miR-203 and BIRC5 siRNA signicantly inhibited cell proliferation in TNBC cells; Moreover up-regulated of BIRC5 and LASP1 was able to abrogate the effects induced by transfection with the miR-203 precursor;miR 203 is a predictive biomarker for colorectal cancer and its expression is associated with BIRC5; The purpose of this study was to explore the role of miR-203 in colorectal cancer CRC and evaluate the correlation between miR-203 and BIRC5; Finally miR-203 expression was negatively associated with that of BIRC5 r = -0.8150 P < 0.05 |
32 | hsa-miR-218-5p | BIRC5 | -0.5 | 0.03986 | 4.5 | 0 | miRTarBase | -0.14 | 0.03933 | 25473903; 25900794; 26442524 | Survivin BIRC5 was subsequently identified as an important cervical cancer target of miR-218 using in silico prediction mRNA profiling and quantitative real-time PCR qRT-PCR;miR-218 binds survivin BIRC5 mRNA 3'-UTR and down-regulated reporter luciferase activity;MiR-218 promoted apoptosis inhibited cell proliferation and caused cell cycle arrest in CRC cells by suppressing BIRC5 expression; In conclusion we demonstrated that high miR-218 expression had a positive prognostic value in 5-FU-based treatments for CRC patients and discovered a novel mechanism mediated by miR-218 to promote apoptosis and to function synergistically with 5-FU to promote chemosensitivity by suppressing BIRC5 and TS in CRC |
33 | hsa-miR-30c-5p | BIRC5 | -0.43 | 0.00016 | 4.5 | 0 | miRNAWalker2 validate | -0.45 | 0.00191 | NA | |
34 | hsa-miR-335-5p | BIRC5 | -1.61 | 0 | 4.5 | 0 | miRNAWalker2 validate | -0.5 | 0 | 23232114 | Genetic variation in a miR 335 binding site in BIRC5 alters susceptibility to lung cancer in Chinese Han populations; In support of the postulation that the 3' UTR SNP may directly affect miRNA-binding site reporter gene assays indicated BIRC5 was a direct target of miR-335 and the rs2239680 T>C change resulted in altered regulation of BIRC5 expression; Our findings defined a 3' UTR SNP in human BIRC5 oncogene that may increase individual susceptibility to lung cancer probably by attenuating the interaction between miR-335 and BIRC5 |
35 | hsa-miR-542-3p | BIRC5 | -1.31 | 0 | 4.5 | 0 | miRNAWalker2 validate | -0.82 | 0 | NA | |
36 | hsa-miR-192-5p | BLM | -0.5 | 0.00345 | 2.51 | 0 | miRNAWalker2 validate | -0.2 | 0.00541 | NA | |
37 | hsa-miR-192-5p | BMP2K | -0.5 | 0.00345 | -0.82 | 0 | miRNAWalker2 validate | -0.16 | 1.0E-5 | NA | |
38 | hsa-miR-20a-5p | BMPR2 | 0.85 | 0 | -0.74 | 0 | miRNAWalker2 validate; miRTarBase | -0.24 | 0 | NA | |
39 | hsa-miR-148a-3p | BTBD3 | -0.75 | 0 | 0.3 | 0.00861 | miRNAWalker2 validate | -0.17 | 1.0E-5 | NA | |
40 | hsa-miR-192-5p | BTF3L4 | -0.5 | 0.00345 | -0.1 | 0.17207 | miRNAWalker2 validate | -0.12 | 0 | NA | |
41 | hsa-miR-20a-5p | BTN3A1 | 0.85 | 0 | 0.33 | 0.01478 | miRNAWalker2 validate | -0.21 | 0 | NA | |
42 | hsa-miR-192-5p | BUB1B | -0.5 | 0.00345 | 3.86 | 0 | miRNAWalker2 validate | -0.22 | 0.01192 | NA | |
43 | hsa-miR-193b-3p | BUB1B | -0.17 | 0.27202 | 3.86 | 0 | miRNAWalker2 validate | -0.2 | 0.04744 | NA | |
44 | hsa-miR-215-5p | BUB1B | -0.98 | 3.0E-5 | 3.86 | 0 | miRNAWalker2 validate | -0.16 | 0.00993 | NA | |
45 | hsa-miR-22-3p | BUB1B | -0.63 | 0 | 3.86 | 0 | miRNAWalker2 validate | -1.6 | 0 | NA | |
46 | hsa-miR-192-5p | CA8 | -0.5 | 0.00345 | 1.3 | 1.0E-5 | miRNAWalker2 validate | -0.35 | 2.0E-5 | NA | |
47 | hsa-miR-192-5p | CAB39L | -0.5 | 0.00345 | -0.5 | 1.0E-5 | miRNAWalker2 validate | -0.17 | 0 | NA | |
48 | hsa-miR-27b-3p | CALM3 | -0.82 | 0 | 0.21 | 0.01527 | miRNAWalker2 validate | -0.11 | 0.00372 | NA | |
49 | hsa-miR-192-5p | CCL3L1 | -0.5 | 0.00345 | -0.81 | 0.00488 | miRNAWalker2 validate | -0.28 | 0.00055 | NA | |
50 | hsa-let-7b-5p | CCNA2 | -0.96 | 0 | 3.37 | 0 | miRNAWalker2 validate; miRTarBase | -0.52 | 0 | NA | |
51 | hsa-let-7b-5p | CCNB1 | -0.96 | 0 | 3.16 | 0 | miRNAWalker2 validate | -0.54 | 0 | NA | |
52 | hsa-miR-20a-5p | CCND1 | 0.85 | 0 | -0.9 | 1.0E-5 | miRNAWalker2 validate; miRTarBase | -0.33 | 0 | NA | |
53 | hsa-miR-20a-5p | CCND2 | 0.85 | 0 | 0.36 | 0.03656 | miRNAWalker2 validate; miRTarBase | -0.16 | 0.00121 | NA | |
54 | hsa-miR-27b-3p | CCND3 | -0.82 | 0 | 0.08 | 0.47843 | miRNAWalker2 validate | -0.24 | 0 | NA | |
55 | hsa-miR-192-5p | CCNE1 | -0.5 | 0.00345 | 3.05 | 0 | miRNAWalker2 validate | -0.35 | 2.0E-5 | NA | |
56 | hsa-miR-192-5p | CCNO | -0.5 | 0.00345 | 1.79 | 2.0E-5 | miRNAWalker2 validate | -0.51 | 2.0E-5 | NA | |
57 | hsa-miR-192-5p | CD83 | -0.5 | 0.00345 | -0.75 | 0 | miRNAWalker2 validate | -0.16 | 0.00018 | NA | |
58 | hsa-miR-192-5p | CDC20 | -0.5 | 0.00345 | 4.44 | 0 | miRNAWalker2 validate | -0.26 | 0.00747 | NA | |
59 | hsa-miR-215-5p | CDC20 | -0.98 | 3.0E-5 | 4.44 | 0 | miRNAWalker2 validate | -0.21 | 0.0025 | NA | |
60 | hsa-miR-23b-3p | CDC20 | -0.53 | 0 | 4.44 | 0 | miRNAWalker2 validate | -0.73 | 0 | NA | |
61 | hsa-miR-30a-5p | CDC20 | -0.63 | 0.00011 | 4.44 | 0 | miRNAWalker2 validate | -0.69 | 0 | NA | |
62 | hsa-miR-29c-3p | CDC23 | -1.44 | 0 | 0.46 | 0 | miRNAWalker2 validate | -0.14 | 0 | NA | |
63 | hsa-miR-148a-3p | CDC25B | -0.75 | 0 | 0.8 | 0 | miRNAWalker2 validate | -0.29 | 0 | 25341915 | Gene CDC25B might be the target gene of miR-148a according to the results of targetscan; CDC25B may be the target gene of miR-148a that plays a role in tumor suppressor |
64 | hsa-miR-192-5p | CDC7 | -0.5 | 0.00345 | 2.02 | 0 | miRNAWalker2 validate | -0.2 | 0.00036 | NA | |
65 | hsa-miR-192-5p | CDCA4 | -0.5 | 0.00345 | 1.27 | 0 | miRNAWalker2 validate | -0.17 | 1.0E-5 | NA | |
66 | hsa-miR-193b-3p | CDK1 | -0.17 | 0.27202 | 3.6 | 0 | miRNAWalker2 validate | -0.25 | 0.00582 | NA | |
67 | hsa-miR-148a-3p | CDK19 | -0.75 | 0 | 0.12 | 0.29406 | miRNAWalker2 validate | -0.24 | 0 | NA | |
68 | hsa-miR-20a-5p | CDKN1A | 0.85 | 0 | -0.77 | 6.0E-5 | miRNAWalker2 validate; miRTarBase | -0.28 | 0 | 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 |
69 | hsa-miR-181a-5p | CDKN1B | 0.25 | 0.05519 | -0.23 | 0.00482 | miRNAWalker2 validate; miRTarBase | -0.13 | 1.0E-5 | NA | |
70 | hsa-miR-221-3p | CDKN1B | 1.12 | 0 | -0.23 | 0.00482 | miRNAWalker2 validate; miRTarBase | -0.15 | 0 | 20146005; 23637992; 19953484; 23939688; 19126397; 23967190; 17569667; 22992757; 17721077; 20461750 | Matched HCC and adjacent non-cancerous samples were assayed for the expression of miR-221 and three G1/S transition inhibitors: p27Kip1 p21WAF1/Cip1and TGF-β1 by in situ hybridization and immunohistochemistry respectively; Real time qRT-PCR was used to investigate miR-221 and p27Kip1 transcripts in different clinical stages; In result miR-221 and TGF-β1 are frequently up-regulated in HCC while p27Kip1 and p21WAF1/Cip1 proteins are frequently down-regulated; In conclusion miR-221 is important in tumorigenesis of HCC possibly by specifically down-regulating p27Kip1 a cell-cycle inhibitor;miR-221 knockdown not only blocked cell cycle progression induced cell apoptosis and inhibited cell proliferation in-vitro but it also inhibited in-vivo tumor growth by targeting p27kip1;Based on bioinformatic analysis we found that the seed sequences of miR-221 and miR-222 coincide with each other and p27kip1 is a target for miRNA-221/222;A Slug/miR-221 network has been suggested linking miR-221 activity with the downregulation of a Slug repressor leading to Slug/miR-221 upregulation and p27Kip1 downregulation; Interference with this process can be achieved using antisense miRNA antagomiR molecules targeting miR-221 inducing the downregulation of Slug and the upregulation of p27Kip1;Moreover a series of functional assays demonstrated that mir-221 could directly inhibit cKit p27Kip1 and possibly other pivotal proteins in melanoma;Additionally the PDGF-dependent increase in cell proliferation appears to be mediated by inhibition of a specific target of miR-221 and down-regulation of p27Kip1;miR 221 and miR 222 expression affects the proliferation potential of human prostate carcinoma cell lines by targeting p27Kip1; In all cell lines tested we show an inverse relationship between the expression of miR-221 and miR-222 and the cell cycle inhibitor p27Kip1; Consistently miR-221 and miR-222 knock-down through antisense LNA oligonucleotides increases p27Kip1 in PC3 cells and strongly reduces their clonogenicity in vitro;Peptide nucleic acids targeting miR 221 modulate p27Kip1 expression in breast cancer MDA MB 231 cells; Targeting miR-221 by PNA resulted in i lowering of the hybridization levels of miR-221 measured by RT-qPCR ii upregulation of p27Kip1 gene expression measured by RT-qPCR and western blot analysis;Antagonism of either microRNA 221 or 222 in glioblastoma cells also caused an increase in p27Kip1 levels and enhanced expression of the luciferase reporter gene fused to the p27Kip1 3'UTR;MiR 221 and MiR 222 alterations in sporadic ovarian carcinoma: Relationship to CDKN1B CDKNIC and overall survival; miR-221 and miR-222 negatively regulate expression of CDKN1B p27 and CDKN1C p57 two cell cycle regulators expressed in ovarian surface epithelium and down-regulated in ovarian carcinomas; In contrast CDKN1B expression was not associated with miR-221 or miR-222 expression |
71 | hsa-miR-222-3p | CDKN1B | 1.09 | 0 | -0.23 | 0.00482 | miRNAWalker2 validate; miRTarBase | -0.14 | 0 | 19953484; 26912358; 24895988; 24137356; 17569667; 27282281; 20461750 | Based on bioinformatic analysis we found that the seed sequences of miR-221 and miR-222 coincide with each other and p27kip1 is a target for miRNA-221/222;Besides microvesicle marker characterization we evidenced that miR-222 exosomal expression mostly reflected its abundance in the cells of origin correctly paralleled by repression of its target genes such as p27Kip1 and induction of the PI3K/AKT pathway thus confirming its functional implication in cancer;MiR-222 plays an important role in the tumorigenesis of CC possibly by specifically down-regulating p27Kip1 and PTEN;miR 222 is upregulated in epithelial ovarian cancer and promotes cell proliferation by downregulating P27kip1; miR-222 upregulation induced an enhancement of ovarian cancer cell proliferation potential possibly by downregulating its target P27Kip1; A bioinformatic analysis showed that the 3'-UTR of the P27Kip1 mRNA contained a highly-conserved putative miR-222 binding site; Luciferase reporter assays demonstrated that P27Kip1 was a direct target of miR-222; Consistently there was an inverse correlation between the P27Kip1 and miR-222 expression levels in the ovarian cancer cell lines and tissues;miR 221 and miR 222 expression affects the proliferation potential of human prostate carcinoma cell lines by targeting p27Kip1; In all cell lines tested we show an inverse relationship between the expression of miR-221 and miR-222 and the cell cycle inhibitor p27Kip1; Consistently miR-221 and miR-222 knock-down through antisense LNA oligonucleotides increases p27Kip1 in PC3 cells and strongly reduces their clonogenicity in vitro;miR 222 confers the resistance of breast cancer cells to Adriamycin through suppression of p27kip1 expression; Immunofluorescence showed that miR-222 altered the subcellular location of p27kip1 in nucleus; The results showed that downregulation of miR-222 in MCF-7/Adr increased sensitivity to Adr and Adr-induced apoptosis and arrested the cells in G1 phase accompanied by more expressions of p27kip1 especially in nucleus; Taken together the results found that miR-222 induced Adr-resistance at least in part via suppressing p27kip1 expression and altering its subcellular localization and miR-222 inhibitors could reverse Adr-resistance of breast cancer cells;MiR 221 and MiR 222 alterations in sporadic ovarian carcinoma: Relationship to CDKN1B CDKNIC and overall survival; miR-221 and miR-222 negatively regulate expression of CDKN1B p27 and CDKN1C p57 two cell cycle regulators expressed in ovarian surface epithelium and down-regulated in ovarian carcinomas; In contrast CDKN1B expression was not associated with miR-221 or miR-222 expression |
72 | hsa-miR-24-3p | CDKN1B | -0.26 | 0.0069 | -0.23 | 0.00482 | miRNAWalker2 validate | -0.13 | 0.00294 | 26847530; 26044523 | The biological significance of miR-24 expression in prostate cancer cells was assessed by a series of in vitro bioassays and the effect on proposed targets p27 CDKN1B and p16 CDK2NA was investigated;With the bioinformatic method we further identified that p27Kip1 is a direct target of miR-24-3p and its protein level was negatively regulated by miR-24-3p |
73 | hsa-miR-98-5p | CDKN1B | -0.05 | 0.71591 | -0.23 | 0.00482 | miRNAWalker2 validate | -0.15 | 0 | NA | |
74 | hsa-miR-192-5p | CDKN2D | -0.5 | 0.00345 | 0.29 | 0.00931 | miRNAWalker2 validate | -0.14 | 1.0E-5 | NA | |
75 | hsa-miR-192-5p | CENPA | -0.5 | 0.00345 | 3.97 | 0 | miRNAWalker2 validate | -0.21 | 0.02088 | NA | |
76 | hsa-miR-192-5p | CENPE | -0.5 | 0.00345 | 3.34 | 0 | miRNAWalker2 validate | -0.17 | 0.02835 | NA | |
77 | hsa-miR-192-5p | CENPF | -0.5 | 0.00345 | 3.79 | 0 | miRNAWalker2 validate | -0.18 | 0.02849 | NA | |
78 | hsa-miR-192-5p | CENPI | -0.5 | 0.00345 | 3.2 | 0 | miRNAWalker2 validate | -0.23 | 0.0096 | NA | |
79 | hsa-miR-192-5p | CEP55 | -0.5 | 0.00345 | 2.87 | 0 | miRNAWalker2 validate | -0.39 | 0 | NA | |
80 | hsa-miR-192-5p | CHST12 | -0.5 | 0.00345 | 0.22 | 0.0166 | miRNAWalker2 validate | -0.23 | 0 | NA | |
81 | hsa-miR-192-5p | CHSY3 | -0.5 | 0.00345 | -1.17 | 0 | miRNAWalker2 validate | -0.2 | 0.00074 | NA | |
82 | hsa-miR-15a-5p | CHUK | 0.35 | 0.00077 | -0.2 | 0.00863 | miRNAWalker2 validate; miRTarBase | -0.12 | 0.00057 | NA | |
83 | hsa-miR-16-5p | CHUK | -0.4 | 0.0001 | -0.2 | 0.00863 | miRNAWalker2 validate; miRTarBase | -0.15 | 3.0E-5 | NA | |
84 | hsa-miR-192-5p | CIB2 | -0.5 | 0.00345 | 1.05 | 9.0E-5 | miRNAWalker2 validate | -0.38 | 0 | NA | |
85 | hsa-miR-192-5p | CKAP4 | -0.5 | 0.00345 | 0.83 | 0 | miRNAWalker2 validate | -0.15 | 2.0E-5 | NA | |
86 | hsa-miR-192-5p | CLIC1 | -0.5 | 0.00345 | 0.77 | 0 | miRNAWalker2 validate | -0.23 | 0 | NA | |
87 | hsa-miR-192-5p | CLIP4 | -0.5 | 0.00345 | -0.22 | 0.43954 | miRNAWalker2 validate | -0.38 | 0 | NA | |
88 | hsa-miR-192-5p | CLSPN | -0.5 | 0.00345 | 2.8 | 0 | miRNAWalker2 validate | -0.3 | 0.00091 | NA | |
89 | hsa-miR-192-5p | CLSTN1 | -0.5 | 0.00345 | 0.33 | 0.03514 | miRNAWalker2 validate | -0.34 | 0 | NA | |
90 | hsa-miR-192-5p | CORO2B | -0.5 | 0.00345 | -0.78 | 0.00171 | miRNAWalker2 validate | -0.37 | 0 | NA | |
91 | hsa-miR-20a-5p | CRIM1 | 0.85 | 0 | -0.43 | 0.03963 | miRTarBase | -0.44 | 0 | NA | |
92 | hsa-miR-331-3p | CTNNB1 | -0.28 | 0.03738 | 0 | 0.98356 | miRNAWalker2 validate | -0.11 | 0.00027 | NA | |
93 | hsa-miR-27a-3p | CUL1 | -0.37 | 0.00876 | -0.12 | 0.10228 | miRNAWalker2 validate | -0.1 | 4.0E-5 | NA | |
94 | hsa-miR-27b-3p | CUL4B | -0.82 | 0 | 0.32 | 1.0E-5 | miRNAWalker2 validate | -0.11 | 0.00064 | NA | |
95 | hsa-miR-192-5p | DDHD1 | -0.5 | 0.00345 | 0.28 | 0.02196 | miRNAWalker2 validate | -0.13 | 0.00017 | NA | |
96 | hsa-miR-192-5p | DEAF1 | -0.5 | 0.00345 | 0.73 | 0 | miRNAWalker2 validate | -0.12 | 2.0E-5 | NA | |
97 | hsa-miR-192-5p | DEGS1 | -0.5 | 0.00345 | 0.4 | 4.0E-5 | miRNAWalker2 validate | -0.13 | 0 | NA | |
98 | hsa-miR-20a-5p | DLC1 | 0.85 | 0 | -1.42 | 0 | miRNAWalker2 validate | -0.18 | 4.0E-5 | NA | |
99 | hsa-miR-192-5p | DLG5 | -0.5 | 0.00345 | 1.51 | 0 | miRNAWalker2 validate | -0.16 | 0.00078 | NA | |
100 | hsa-miR-192-5p | DLGAP5 | -0.5 | 0.00345 | 4.11 | 0 | miRNAWalker2 validate | -0.2 | 0.02547 | NA | |
101 | hsa-miR-192-5p | DNAJB5 | -0.5 | 0.00345 | 0.37 | 0.00017 | miRNAWalker2 validate | -0.16 | 0 | NA | |
102 | hsa-miR-192-5p | DNAL1 | -0.5 | 0.00345 | -0.09 | 0.30099 | miRNAWalker2 validate | -0.2 | 0 | NA | |
103 | hsa-miR-148a-3p | DNMT1 | -0.75 | 0 | 1.07 | 0 | miRNAWalker2 validate; miRTarBase | -0.22 | 0 | 25865490; 26111756; 25950085; 22167392 | miR 148a dependent apoptosis of bladder cancer cells is mediated in part by the epigenetic modifier DNMT1; We additionally show that miR-148a exerts this effect partially by attenuating expression of DNA methyltransferase 1 DNMT1;Moreover we found that miR-148a appeared to be a target of bufalin and miR-148a further regulated DNMT1 and p27 to control the stemness of OS cells;The Interplay Between miR 148a and DNMT1 Might be Exploited for Pancreatic Cancer Therapy; We discovered the expression level of miR-148a significantly decreased in pancreatic cancer tissues whereas that of DNMT1 increased; In ASPC-1 cancer cells the overexpression of miR-148a led to a decreased level of DNMT1 and reduced the proliferation and metastasis of ASPC-1 cells; Interestingly it was shown that the DNMT1 inhibition enhanced the expression of miR-148a; In vivo studies demonstrated that the tumorigenesis of ASPC-1 was significantly arrested by either the overexpression of miR-148a or the inhibition of DNMT1;Studies have shown that microRNA-148a miR-148a was proved to be silenced while DNA methyltransferase 1 DNMT1 was over-expressed in gastric cancer; But the mechanism of aberrant expression of miR-148a and DNMT1 and their relationships in gastric cancer are still unknown; The aims of this study were to investigate the expression profile of miR-148a and DNMT1 and reveal whether they have any relationships; We used reverse-transcriptase quantitative real-time PCR methylation-specific PCR and Western blot to measure the level of miR-148a expression DNA methylation level and DNMT1 expression respectively; DNMT1 was over-expressed in primary tumors and cell lines while knockdown of DNMT1 using siRNA could decrease methylation level of miR-148a promoter and restore its expression; Furthermore ectopic over-expression of miR-148a in cancer cell lines caused reduction in DNMT1 expression and inhibited cell proliferation but no obvious change was found in apoptosis rate; These results suggest that miR-148a is inactivated by DNA hypermethylation of promoter region in gastric cancer which is mediated through DNMT1 over-expression; Additionally the silence of miR-148a reduces its suppression to DNMT1 in gastric cancer and this may in turn result in over-expression of DNMT1 and promote DNA hypermethylation |
104 | hsa-miR-148a-3p | DNMT3B | -0.75 | 0 | 1.62 | 0 | miRNAWalker2 validate; miRTarBase | -0.19 | 0.00195 | 20841507 | Low ERG expressers presented with down-regulation of genes involved in the DNA-methylation machinery and up-regulation of miR-148a which targets DNMT3B |
105 | hsa-miR-148a-3p | DSTYK | -0.75 | 0 | 1.01 | 0 | miRNAWalker2 validate | -0.2 | 0 | NA | |
106 | hsa-miR-192-5p | DSTYK | -0.5 | 0.00345 | 1.01 | 0 | miRNAWalker2 validate | -0.27 | 0 | NA | |
107 | hsa-miR-192-5p | E2F5 | -0.5 | 0.00345 | 0.73 | 0.0004 | miRNAWalker2 validate | -0.17 | 0.00489 | NA | |
108 | hsa-miR-192-5p | ECT2 | -0.5 | 0.00345 | 2.35 | 0 | miRNAWalker2 validate | -0.23 | 0.00021 | NA | |
109 | hsa-miR-192-5p | EEF1A2 | -0.5 | 0.00345 | 3.15 | 0 | miRNAWalker2 validate | -0.44 | 0.01793 | NA | |
110 | hsa-miR-192-5p | EFNB2 | -0.5 | 0.00345 | 0.1 | 0.47703 | miRNAWalker2 validate | -0.17 | 2.0E-5 | NA | |
111 | hsa-miR-146a-5p | EGFR | -0.74 | 0.00077 | -1.02 | 0 | miRNAWalker2 validate | -0.22 | 0 | 24895573; 25242818; 22161865; 25596948; 25417703; 23555954; 24839931; 21632853 | Furthermore western blot showed that miR-146a mimic downregulated EGFR ERK1/2 and stat5 signalings; These effects were less potent compared to that of a siRNA targeting EGFR a known target gene of miR-146a; Moreover miR-146a mimic could enhance the cell growth inhibition and apoptosis induction impact of various EGFR targeting agents;Interestingly re-expression of miR-146a inhibited the invasive capacity of Colo357 and Panc-1 PC cells with concomitant down-regulation of EGFR and IRAK-1; Most importantly we found that the treatment of PC cells with "natural agents" 33'-diinodolylmethane DIM or isoflavone led to an increase in the expression of miR-146a and consequently down-regulated the expression of EGFR MTA-2 IRAK-1 and NF-κB resulting in the inhibition of invasion of Colo357 and Panc-1 cells;MiR 146a suppresses tumor growth and progression by targeting EGFR pathway and in a p ERK dependent manner in castration resistant prostate cancer; Mechanistic studies revealed that miR-146a repressed the expression of EGFR through binding to its 3'-untranslated region; Our findings suggest that ubiquitous loss of miR-146a is a critical mechanism for overexpression of EGFR in CRPC which is crucial to better understanding the pathogenesis of CRPC;Furthermore the expressions of bax and cleaved-caspase-3 mainly were increased in control and overexpression miR-146a groups however the expression of EGFR was inverse; All the results demonstrated that quercetin exhibited excellent effect on inhibiting cell proliferation in human breast cancer cells which was performed by up-regulating miR-146a expression then via inducing apoptosis through caspase-3 activation and mitochondrial-dependent pathways and inhibiting invasion through down-regulating the expression of EGFR;Here we report a previously unrecognized posttranscriptional mechanism by which BRCA1 regulates EGFR expression through the induction of miR-146a; We show that BRCA1 binds to MIR146A promoter and activates transcription which in turn attenuates EGFR expression;In functional experiments miR-146a suppressed cell growth induced cellular apoptosis and inhibited EGFR downstream signaling in five NSCLC cell lines H358 H1650 H1975 HCC827 and H292 miR-146a also inhibited the migratory capacity of these NSCLC cells; On the other hand miR-146a enhanced the inhibition of cell proliferation by drugs targeting EGFR including both TKIs gefitinib erlotinib and afatinib and a monoclonal antibody cetuximab; Our results suggest that these effects of miR-146a are due to its targeting of EGFR and NF-κB signaling;Deregulation of miR 146a expression in a mouse model of pancreatic cancer affecting EGFR signaling; Treatment of PC cells with CDF a novel synthetic compound led to re-expression of miR-146a resulting in the down-regulation of EGFR expression; Further knock-down of miR-146a in AsPC-1 cells led to the up-regulation of EGFR expression and showed increased clonogenic growth; In addition knock-down of EGFR by EGFR siRNA transfection of parental AsPC-1 cells and AsPC-1 cells stably transfected with pre-miR-146a resulted in decreased invasive capacity which was further confirmed by reduced luciferase activity in cells transfected with pMIR-Luc reporter vector containing miR-146a binding site; Collectively these results suggest that the loss of expression of miR-146a is a fundamental mechanism for over-expression of EGFR signaling and that re-expression of miR-146a by CDF treatment could be useful in designing personalized strategy for the treatment of human PC;The regulation of EGFR and IRAK1 by miR-146a was examined with miR-146a-transfected gastric cancer cells; Ectopic expression of miR-146a inhibited migration and invasion and downregulated EGFR and IRAK1 expression in gastric cancer cells; MiR-146a targeting of EGFR and IRAK1 is an independent prognostic factor in gastric cancer cases |
112 | hsa-miR-155-5p | EGFR | 0.01 | 0.95651 | -1.02 | 0 | miRNAWalker2 validate | -0.13 | 0.01158 | NA | |
113 | hsa-miR-17-5p | EGFR | 0.7 | 2.0E-5 | -1.02 | 0 | TargetScan | -0.16 | 0.00764 | NA | |
114 | hsa-miR-21-5p | EGFR | 1.51 | 0 | -1.02 | 0 | miRNAWalker2 validate; miRTarBase | -0.44 | 0 | 24198203; 20113523; 24012640; 24331411; 26563758; 19597153; 26026961; 20048743 | In radically resected NSCLC patients the expression levels of miR-21 10b in patients with EGFR mutation were much higher than those without mutation;Thus the miR-21 inhibitor might interrupt the activity of EGFR pathways independently of PTEN status;Further the expression of miR-21 is regulated by EGFR via the activation of β-catenin and AP-1; These data indicate that a feedback loop exists between miR-21 and EGFR; These results clarify a novel association between miR-21 and EGFR in the regulation of cancer cell progression;MiR 21 overexpression is associated with acquired resistance of EGFR TKI in non small cell lung cancer;Higher expression levels of miR-21 AmiR-27a and miR-218 detected in this study suggest potential roles of these miRNAs in primary resistance to EGFR-TKI in advanced NSCLC patients with EGFR exon 19 deletion mutations;MiR 21 is an EGFR regulated anti apoptotic factor in lung cancer in never smokers; The changes in expression of some of these miRNAs including miR-21 were more remarkable in cases with EGFR mutations than in those without these mutations; In the never-smoker-derived lung adenocarcinoma cell line H3255 with mutant EGFR and high levels of p-EGFR and miR-21 antisense inhibition of miR-21 enhanced AG1478-induced apoptosis; In a never-smoker-derived adenocarcinoma cell line H441 with wild-type EGFR the antisense miR-21 not only showed the additive effect with AG1478 but also induced apoptosis by itself; These results suggest that aberrantly increased expression of miR-21 which is enhanced further by the activated EGFR signaling pathway plays a significant role in lung carcinogenesis in never-smokers as well as in smokers and is a potential therapeutic target in both EGFR-mutant and wild-type cases;Nickel may contribute to EGFR mutation and synergistically promotes tumor invasion in EGFR mutated lung cancer via nickel induced microRNA 21 expression;Downregulation of miR 21 inhibits EGFR pathway and suppresses the growth of human glioblastoma cells independent of PTEN status |
115 | hsa-miR-17-5p | EGLN1 | 0.7 | 2.0E-5 | 0.08 | 0.4055 | TargetScan | -0.1 | 9.0E-5 | NA | |
116 | hsa-miR-192-5p | EHBP1L1 | -0.5 | 0.00345 | 0.33 | 0.00124 | miRNAWalker2 validate | -0.15 | 0 | NA | |
117 | hsa-miR-27b-3p | EHMT2 | -0.82 | 0 | 1.31 | 0 | miRNAWalker2 validate | -0.24 | 0 | NA | |
118 | hsa-miR-192-5p | ELOVL1 | -0.5 | 0.00345 | 0.77 | 0 | miRNAWalker2 validate | -0.13 | 0 | NA | |
119 | hsa-miR-192-5p | EMB | -0.5 | 0.00345 | -0.51 | 0.02271 | miRNAWalker2 validate | -0.47 | 0 | NA | |
120 | hsa-miR-192-5p | EML1 | -0.5 | 0.00345 | -0.63 | 0.00019 | miRNAWalker2 validate | -0.23 | 0 | NA | |
121 | hsa-miR-192-5p | ENC1 | -0.5 | 0.00345 | -1.09 | 0 | miRNAWalker2 validate | -0.17 | 0.00145 | NA | |
122 | hsa-miR-192-5p | ENDOD1 | -0.5 | 0.00345 | -1 | 0 | miRNAWalker2 validate | -0.46 | 0 | NA | |
123 | hsa-miR-192-5p | ENTPD3 | -0.5 | 0.00345 | 0.3 | 0.38056 | miRNAWalker2 validate | -0.52 | 0 | NA | |
124 | hsa-miR-192-5p | EPDR1 | -0.5 | 0.00345 | 0.22 | 0.25962 | miRNAWalker2 validate | -0.26 | 0 | NA | |
125 | hsa-miR-192-5p | ERCC6L | -0.5 | 0.00345 | 2.8 | 0 | miRNAWalker2 validate | -0.14 | 0.04236 | NA | |
126 | hsa-miR-192-5p | ERMP1 | -0.5 | 0.00345 | 0.54 | 1.0E-5 | miRNAWalker2 validate | -0.12 | 0.0003 | NA | |
127 | hsa-miR-221-3p | ETS1 | 1.12 | 0 | -0.89 | 0 | miRTarBase | -0.16 | 0.00028 | 21711453 | To close the loop we demonstrate ETS-1 as a direct target of miR-222 but not miR-221 showing the novel option of their uncoupled functions |
128 | hsa-miR-222-3p | ETS1 | 1.09 | 0 | -0.89 | 0 | miRNAWalker2 validate; miRTarBase | -0.11 | 0.00861 | 21711453 | Constitutive activation of the ETS 1 miR 222 circuitry in metastatic melanoma; We demonstrate that the proto-oncogene ETS-1 involved in the pathogenesis of cancers of different origin is a transcriptional regulator of miR-222 by direct binding to its promoter region; Differently from 293FT cells or early stage melanomas where unphosphorylated ETS-1 represses miR-222 transcription in metastatic melanoma the constitutively Thr-38 phosphorylated fraction of ETS-1 induces miR-222; To close the loop we demonstrate ETS-1 as a direct target of miR-222 but not miR-221 showing the novel option of their uncoupled functions |
129 | hsa-miR-192-5p | FAIM | -0.5 | 0.00345 | 0.59 | 0 | miRNAWalker2 validate | -0.18 | 0 | NA | |
130 | hsa-miR-192-5p | FAM171B | -0.5 | 0.00345 | 0.78 | 0.00013 | miRNAWalker2 validate | -0.49 | 0 | NA | |
131 | hsa-miR-192-5p | FAM189A2 | -0.5 | 0.00345 | -0.05 | 0.82444 | miRNAWalker2 validate | -0.41 | 0 | NA | |
132 | hsa-miR-192-5p | FAM63B | -0.5 | 0.00345 | -0.54 | 0.00241 | miRNAWalker2 validate | -0.11 | 0.0386 | NA | |
133 | hsa-miR-192-5p | FANCI | -0.5 | 0.00345 | 2.59 | 0 | miRNAWalker2 validate | -0.18 | 0.00303 | NA | |
134 | hsa-miR-192-5p | FBN1 | -0.5 | 0.00345 | 0.04 | 0.84475 | miRNAWalker2 validate | -0.45 | 0 | NA | |
135 | hsa-miR-20a-5p | FBXO3 | 0.85 | 0 | -0.54 | 0 | miRNAWalker2 validate | -0.13 | 0 | NA | |
136 | hsa-miR-192-5p | FERMT1 | -0.5 | 0.00345 | 1.15 | 0.00602 | miRNAWalker2 validate | -0.52 | 1.0E-5 | NA | |
137 | hsa-miR-103a-3p | FGF2 | 0.77 | 0 | -1.09 | 0.00032 | miRNAWalker2 validate | -0.33 | 0.01183 | NA | |
138 | hsa-miR-215-5p | FGF2 | -0.98 | 3.0E-5 | -1.09 | 0.00032 | miRNAWalker2 validate | -0.15 | 0.01382 | NA | |
139 | hsa-miR-92a-3p | FGF2 | 0.21 | 0.13429 | -1.09 | 0.00032 | miRNAWalker2 validate | -0.64 | 0 | NA | |
140 | hsa-miR-20a-5p | FGF7 | 0.85 | 0 | -0.65 | 0.00602 | miRNAWalker2 validate | -0.34 | 0 | NA | |
141 | hsa-miR-100-5p | FGFR3 | -0.78 | 0.00022 | 0.19 | 0.3402 | miRNAWalker2 validate; miRTarBase | -0.27 | 0 | 25344675; 26604796; 26018508; 23778527 | MicroRNA 100 regulates pancreatic cancer cells growth and sensitivity to chemotherapy through targeting FGFR3; The predicted target of miR-100 fibroblast growth factor receptor 3 FGFR3 was downregulated by siRNA to examine its effect on pancreatic cancer cells; Luciferase essay showed FGFR3 was direct target of miR-100; FGFR3 was significantly downregulated by overexpressing miR-100 in pancreatic cancer cells and knocking down FGFR3 by siRNA exerted similar effect as miR-100; Our study demonstrated that miR-100 played an important role in pancreatic cancer development possibly through targeting FGFR3;Overexpression of miR 100 inhibits cell proliferation migration and chemosensitivity in human glioblastoma through FGFR3; Expression of fibroblast growth factor receptor 3 FGFR3 the bioinformatically predicted target of miR-100 was examined by Western blot in glioblastoma; FGFR3 was directly regulated by miR-100 in glioblastoma; Ectopically overexpressing FGFR3 was able to ameliorate the anticancer effects of upregulation of miR-100 on glioblastoma growth migration and chemosensitivity; Overexpressing miR-100 had anticancer effects on glioblastoma likely through regulation of FGFR3;Overexpression of miR 100 inhibits growth of osteosarcoma through FGFR3; Here we reported significantly higher levels of fibroblast growth factor receptor 3 FGFR3 and significantly lower levels of miR-100 in the OS specimen compared to those in the paired normal bone tissues; Bioinformatics analysis and luciferase reporter assay suggest that miR-100 binds to the 3'UTR of FGFR3 mRNA to prevent its translation; Taken together our data demonstrate that miR-100 may inhibit the growth of OS through FGFR3;Hypoxia regulates FGFR3 expression via HIF 1α and miR 100 and contributes to cell survival in non muscle invasive bladder cancer; We have previously investigated the role of microRNAs in bladder cancer and have shown that FGFR3 is a target of miR-100; In this study we investigated the effects of hypoxia on miR-100 and FGFR3 expression and the link between miR-100 and FGFR3 in hypoxia; Bladder cancer cell lines were exposed to normoxic or hypoxic conditions and examined for the expression of FGFR3 by quantitative PCR qPCR and western blotting and miR-100 by qPCR; The effect of FGFR3 and miR-100 on cell viability in two-dimensional 2-D and three-dimensional 3-D was examined by transfecting siRNA or mimic-100 respectively; Increased FGFR3 was also in part dependent on miR-100 levels which decreased in hypoxia; Hypoxia in part via suppression of miR-100 induces FGFR3 expression in bladder cancer both of which have an important role in maintaining cell viability under conditions of stress |
142 | hsa-miR-99a-5p | FGFR3 | -1.51 | 0 | 0.19 | 0.3402 | miRNAWalker2 validate; miRTarBase | -0.3 | 0 | 23409016; 24456664; 23298836 | Photofrin based photodynamic therapy and miR 99a transfection inhibited FGFR3 and PI3K/Akt signaling mechanisms to control growth of human glioblastoma In vitro and in vivo; Further photofrin based PDT followed by miR-99a transfection dramatically increased miR-99a expression and also increased apoptosis in glioblastoma cell cultures and drastically reduced tumor growth in athymic nude mice due to down regulation of fibroblast growth factor receptor 3 FGFR3 and PI3K/Akt signaling mechanisms leading to inhibition of cell proliferation and induction of molecular mechanisms of apoptosis;miR 99a promotes proliferation targeting FGFR3 in human epithelial ovarian cancer cells; Importantly fibroblast growth factor receptor 3 FGFR3 predicted to be one target gene of miR-99a using computational algorithms was higher in expression in EOC cells; Subsequently FGFR3 was proved to be direct target of miR-99a by dual luciferase assay; Furthermore overexpression of miR-99a dramatically suppressed expression level of FGFR3 at both mRNA and protein levels proving FGFR3 to be inversely correlated with miR-99a; Finally overexpression of miR-99a could significantly inhibit EOC cell proliferation in vitro by decreasing the expression of FGFR3 which also reduced the EOC cell growth after siRNA knockdown; Conclusively miR-99a expression was remarkably downregulated in serums tissues and cell and suppresses EOC cell proliferation by targeting FGFR3 suggesting miR-99a as a prospective prognosis marker and potential tumor suppressor for EOC therapeutics;The tumorigenic FGFR3 TACC3 gene fusion escapes miR 99a regulation in glioblastoma; The fusion caused by tandem duplication on 4p16.3 led to the loss of the 3'-UTR of FGFR3 blocking gene regulation of miR-99a and enhancing expression of the fusion gene |
143 | hsa-miR-192-5p | FHDC1 | -0.5 | 0.00345 | 1.32 | 0 | miRNAWalker2 validate | -0.44 | 0 | NA | |
144 | hsa-miR-20a-5p | FLNA | 0.85 | 0 | 0.23 | 0.20343 | miRNAWalker2 validate | -0.24 | 0 | NA | |
145 | hsa-miR-192-5p | FUT11 | -0.5 | 0.00345 | -0.32 | 0.01362 | miRNAWalker2 validate | -0.13 | 0.00043 | NA | |
146 | hsa-miR-192-5p | FZD1 | -0.5 | 0.00345 | -0.99 | 0 | miRNAWalker2 validate | -0.46 | 0 | NA | |
147 | hsa-miR-101-3p | FZD6 | -1.48 | 0 | 0.59 | 0.00374 | miRNAWalker2 validate | -0.31 | 1.0E-5 | NA | |
148 | hsa-miR-192-5p | FZD7 | -0.5 | 0.00345 | -0.28 | 0.25656 | miRNAWalker2 validate | -0.59 | 0 | NA | |
149 | hsa-miR-192-5p | GALNT12 | -0.5 | 0.00345 | -0.64 | 0.04377 | miRNAWalker2 validate | -0.39 | 1.0E-5 | NA | |
150 | hsa-miR-148a-3p | GAS1 | -0.75 | 0 | -2.01 | 0 | miRNAWalker2 validate | -0.45 | 0 | NA |
Num | GO | Overlap | Size | P Value | Adj. P Value |
---|---|---|---|---|---|
1 | CELL CYCLE PROCESS | 76 | 1081 | 1.637e-26 | 7.615e-23 |
2 | CELL CYCLE | 82 | 1316 | 3.751e-25 | 8.728e-22 |
3 | MITOTIC CELL CYCLE | 59 | 766 | 1.797e-22 | 2.787e-19 |
4 | REGULATION OF CELL CYCLE | 64 | 949 | 2.715e-21 | 3.158e-18 |
5 | REGULATION OF CELL CYCLE PROCESS | 46 | 558 | 9.017e-19 | 8.392e-16 |
6 | SISTER CHROMATID SEGREGATION | 25 | 176 | 4.57e-16 | 3.544e-13 |
7 | REGULATION OF CELL CYCLE PHASE TRANSITION | 32 | 321 | 1.174e-15 | 7.807e-13 |
8 | POSITIVE REGULATION OF PROTEIN MODIFICATION PROCESS | 60 | 1135 | 5.417e-15 | 3.151e-12 |
9 | CELL DIVISION | 37 | 460 | 6.317e-15 | 3.266e-12 |
10 | POSITIVE REGULATION OF PROTEIN METABOLIC PROCESS | 70 | 1492 | 8.227e-15 | 3.828e-12 |
11 | REGULATION OF PROTEIN MODIFICATION PROCESS | 75 | 1710 | 2.483e-14 | 9.928e-12 |
12 | NUCLEAR CHROMOSOME SEGREGATION | 26 | 228 | 2.56e-14 | 9.928e-12 |
13 | REGULATION OF MITOTIC CELL CYCLE | 36 | 468 | 5.845e-14 | 2.092e-11 |
14 | REGULATION OF CHROMOSOME SEGREGATION | 17 | 85 | 7.53e-14 | 2.503e-11 |
15 | CHROMOSOME SEGREGATION | 27 | 272 | 2.412e-13 | 7.481e-11 |
16 | ORGANELLE FISSION | 36 | 496 | 3.335e-13 | 9.7e-11 |
17 | REGULATION OF TRANSFERASE ACTIVITY | 51 | 946 | 3.786e-13 | 1.036e-10 |
18 | POSITIVE REGULATION OF TRANSFERASE ACTIVITY | 40 | 616 | 5.442e-13 | 1.407e-10 |
19 | NEGATIVE REGULATION OF CELL CYCLE | 33 | 433 | 8.978e-13 | 2.199e-10 |
20 | MITOTIC NUCLEAR DIVISION | 30 | 361 | 1.142e-12 | 2.657e-10 |
21 | REGULATION OF PHOSPHORUS METABOLIC PROCESS | 69 | 1618 | 1.297e-12 | 2.873e-10 |
22 | POSITIVE REGULATION OF CATALYTIC ACTIVITY | 66 | 1518 | 1.877e-12 | 3.97e-10 |
23 | CELL CYCLE PHASE TRANSITION | 25 | 255 | 2.521e-12 | 5.1e-10 |
24 | MITOTIC SISTER CHROMATID SEGREGATION | 16 | 91 | 3.358e-12 | 6.51e-10 |
25 | RESPONSE TO ALCOHOL | 29 | 362 | 6.833e-12 | 1.272e-09 |
26 | SISTER CHROMATID COHESION | 17 | 111 | 7.17e-12 | 1.283e-09 |
27 | NEGATIVE REGULATION OF CELL CYCLE PHASE TRANSITION | 19 | 146 | 8.047e-12 | 1.387e-09 |
28 | POSITIVE REGULATION OF PHOSPHATE METABOLIC PROCESS | 51 | 1036 | 1.131e-11 | 1.814e-09 |
29 | POSITIVE REGULATION OF PHOSPHORUS METABOLIC PROCESS | 51 | 1036 | 1.131e-11 | 1.814e-09 |
30 | CHROMOSOME ORGANIZATION | 50 | 1009 | 1.46e-11 | 2.265e-09 |
31 | PROTEIN PHOSPHORYLATION | 48 | 944 | 1.609e-11 | 2.415e-09 |
32 | POSITIVE REGULATION OF MOLECULAR FUNCTION | 71 | 1791 | 1.756e-11 | 2.554e-09 |
33 | RESPONSE TO ORGANIC CYCLIC COMPOUND | 47 | 917 | 2.046e-11 | 2.885e-09 |
34 | POSITIVE REGULATION OF CELL CYCLE | 27 | 332 | 2.647e-11 | 3.622e-09 |
35 | MITOTIC CELL CYCLE CHECKPOINT | 18 | 139 | 3.135e-11 | 4.167e-09 |
36 | NEGATIVE REGULATION OF MITOTIC CELL CYCLE | 21 | 199 | 3.708e-11 | 4.793e-09 |
37 | REGULATION OF CELL DIVISION | 24 | 272 | 6.48e-11 | 8.149e-09 |
38 | REGULATION OF CELL PROLIFERATION | 62 | 1496 | 7.388e-11 | 9.046e-09 |
39 | MORPHOGENESIS OF AN EPITHELIUM | 29 | 400 | 7.664e-11 | 9.144e-09 |
40 | REGULATION OF SISTER CHROMATID SEGREGATION | 13 | 67 | 1.012e-10 | 1.177e-08 |
41 | TUBE DEVELOPMENT | 34 | 552 | 1.392e-10 | 1.579e-08 |
42 | NEGATIVE REGULATION OF CELL CYCLE PROCESS | 21 | 214 | 1.462e-10 | 1.619e-08 |
43 | CELL CYCLE CHECKPOINT | 20 | 194 | 1.67e-10 | 1.807e-08 |
44 | EPITHELIUM DEVELOPMENT | 46 | 945 | 1.894e-10 | 2.003e-08 |
45 | REGULATION OF MICROTUBULE BASED PROCESS | 22 | 243 | 2.523e-10 | 2.609e-08 |
46 | POSITIVE REGULATION OF CELL CYCLE PROCESS | 22 | 247 | 3.452e-10 | 3.491e-08 |
47 | MICROTUBULE CYTOSKELETON ORGANIZATION | 26 | 348 | 3.987e-10 | 3.947e-08 |
48 | CELL PROLIFERATION | 37 | 672 | 4.822e-10 | 4.674e-08 |
49 | REGULATION OF KINASE ACTIVITY | 40 | 776 | 6.292e-10 | 5.975e-08 |
50 | PROTEIN LOCALIZATION TO CHROMOSOME CENTROMERIC REGION | 7 | 13 | 6.581e-10 | 6.124e-08 |
51 | CELL CYCLE G1 S PHASE TRANSITION | 15 | 111 | 7.695e-10 | 6.885e-08 |
52 | G1 S TRANSITION OF MITOTIC CELL CYCLE | 15 | 111 | 7.695e-10 | 6.885e-08 |
53 | TISSUE MORPHOGENESIS | 32 | 533 | 9.451e-10 | 8.297e-08 |
54 | REGULATION OF ORGANELLE ORGANIZATION | 51 | 1178 | 1.07e-09 | 9.216e-08 |
55 | RESPONSE TO ENDOGENOUS STIMULUS | 58 | 1450 | 1.293e-09 | 1.094e-07 |
56 | CYTOSKELETON ORGANIZATION | 41 | 838 | 1.754e-09 | 1.457e-07 |
57 | RESPONSE TO DRUG | 28 | 431 | 1.975e-09 | 1.612e-07 |
58 | MITOTIC SPINDLE ORGANIZATION | 12 | 69 | 2.027e-09 | 1.626e-07 |
59 | MICROTUBULE BASED PROCESS | 31 | 522 | 2.274e-09 | 1.794e-07 |
60 | PHOSPHORYLATION | 51 | 1228 | 4.354e-09 | 3.377e-07 |
61 | REGULATION OF CELL CYCLE G2 M PHASE TRANSITION | 11 | 59 | 4.452e-09 | 3.396e-07 |
62 | REGULATION OF EPITHELIAL CELL PROLIFERATION | 22 | 285 | 5.074e-09 | 3.808e-07 |
63 | POSITIVE REGULATION OF KINASE ACTIVITY | 29 | 482 | 5.731e-09 | 4.233e-07 |
64 | SPINDLE CHECKPOINT | 8 | 25 | 5.92e-09 | 4.263e-07 |
65 | REGULATION OF MULTICELLULAR ORGANISMAL DEVELOPMENT | 62 | 1672 | 5.955e-09 | 4.263e-07 |
66 | TISSUE DEVELOPMENT | 58 | 1518 | 6.953e-09 | 4.902e-07 |
67 | RESPONSE TO ABIOTIC STIMULUS | 45 | 1024 | 7.373e-09 | 5.121e-07 |
68 | POSITIVE REGULATION OF CELL PROLIFERATION | 39 | 814 | 8.059e-09 | 5.515e-07 |
69 | CELLULAR RESPONSE TO ORGANIC CYCLIC COMPOUND | 28 | 465 | 1.043e-08 | 7.031e-07 |
70 | REGULATION OF CYCLIN DEPENDENT PROTEIN KINASE ACTIVITY | 13 | 97 | 1.169e-08 | 7.772e-07 |
71 | RESPONSE TO GROWTH FACTOR | 28 | 475 | 1.648e-08 | 1.08e-06 |
72 | PHOSPHATE CONTAINING COMPOUND METABOLIC PROCESS | 68 | 1977 | 1.959e-08 | 1.266e-06 |
73 | REGULATION OF CELL DIFFERENTIATION | 56 | 1492 | 2.455e-08 | 1.565e-06 |
74 | TUBE MORPHOGENESIS | 22 | 323 | 4.869e-08 | 3.062e-06 |
75 | ORGAN MORPHOGENESIS | 38 | 841 | 5.931e-08 | 3.68e-06 |
76 | POSITIVE REGULATION OF DEVELOPMENTAL PROCESS | 46 | 1142 | 6.82e-08 | 4.175e-06 |
77 | CHROMOSOME LOCALIZATION | 10 | 61 | 8.237e-08 | 4.851e-06 |
78 | REGULATION OF CHROMOSOME ORGANIZATION | 20 | 278 | 8.229e-08 | 4.851e-06 |
79 | REGULATION OF MICROTUBULE POLYMERIZATION OR DEPOLYMERIZATION | 16 | 178 | 8.081e-08 | 4.851e-06 |
80 | CELLULAR RESPONSE TO ALCOHOL | 13 | 115 | 9.283e-08 | 5.399e-06 |
81 | RESPONSE TO NITROGEN COMPOUND | 38 | 859 | 1.022e-07 | 5.828e-06 |
82 | MOVEMENT OF CELL OR SUBCELLULAR COMPONENT | 49 | 1275 | 1.027e-07 | 5.828e-06 |
83 | CELLULAR RESPONSE TO ENDOGENOUS STIMULUS | 42 | 1008 | 1.08e-07 | 6.053e-06 |
84 | POSITIVE REGULATION OF CYCLIN DEPENDENT PROTEIN KINASE ACTIVITY | 8 | 36 | 1.404e-07 | 7.778e-06 |
85 | CELL MOTILITY | 37 | 835 | 1.463e-07 | 7.914e-06 |
86 | LOCALIZATION OF CELL | 37 | 835 | 1.463e-07 | 7.914e-06 |
87 | RESPONSE TO OXYGEN CONTAINING COMPOUND | 51 | 1381 | 1.885e-07 | 1.005e-05 |
88 | REGULATION OF PROTEIN SERINE THREONINE KINASE ACTIVITY | 26 | 470 | 1.901e-07 | 1.005e-05 |
89 | CYTOKINESIS | 11 | 84 | 2.014e-07 | 1.053e-05 |
90 | RESPONSE TO IONIZING RADIATION | 14 | 145 | 2.18e-07 | 1.127e-05 |
91 | CELLULAR RESPONSE TO ORGANIC SUBSTANCE | 62 | 1848 | 2.298e-07 | 1.175e-05 |
92 | RESPONSE TO RADIATION | 24 | 413 | 2.337e-07 | 1.182e-05 |
93 | RESPONSE TO INORGANIC SUBSTANCE | 26 | 479 | 2.741e-07 | 1.357e-05 |
94 | CYTOSKELETON DEPENDENT CYTOKINESIS | 8 | 39 | 2.729e-07 | 1.357e-05 |
95 | NEGATIVE REGULATION OF CELLULAR COMPONENT ORGANIZATION | 32 | 684 | 3.282e-07 | 1.607e-05 |
96 | NEGATIVE REGULATION OF GENE EXPRESSION | 53 | 1493 | 3.633e-07 | 1.761e-05 |
97 | REGULATION OF ANATOMICAL STRUCTURE MORPHOGENESIS | 41 | 1021 | 4.107e-07 | 1.97e-05 |
98 | CELL CYCLE ARREST | 14 | 154 | 4.582e-07 | 2.175e-05 |
99 | PROTEIN LOCALIZATION TO KINETOCHORE | 5 | 11 | 6.206e-07 | 2.887e-05 |
100 | REGULATION OF ATTACHMENT OF SPINDLE MICROTUBULES TO KINETOCHORE | 5 | 11 | 6.206e-07 | 2.887e-05 |
101 | RESPONSE TO LIPID | 37 | 888 | 6.582e-07 | 3.032e-05 |
102 | MITOTIC CYTOKINESIS | 7 | 31 | 7.724e-07 | 3.524e-05 |
103 | NEGATIVE REGULATION OF CELL DIVISION | 9 | 60 | 8.107e-07 | 3.662e-05 |
104 | PROTEIN LOCALIZATION TO CHROMOSOME | 8 | 45 | 8.741e-07 | 3.911e-05 |
105 | REGULATION OF NUCLEAR DIVISION | 14 | 163 | 9.141e-07 | 4.051e-05 |
106 | NEGATIVE REGULATION OF ORGANELLE ORGANIZATION | 22 | 387 | 1.084e-06 | 4.757e-05 |
107 | POSITIVE REGULATION OF LOCOMOTION | 23 | 420 | 1.17e-06 | 5.086e-05 |
108 | CELLULAR RESPONSE TO OXYGEN CONTAINING COMPOUND | 34 | 799 | 1.208e-06 | 5.108e-05 |
109 | MITOTIC DNA INTEGRITY CHECKPOINT | 11 | 100 | 1.202e-06 | 5.108e-05 |
110 | REGULATION OF PROTEIN COMPLEX DISASSEMBLY | 16 | 217 | 1.194e-06 | 5.108e-05 |
111 | NEGATIVE REGULATION OF NITROGEN COMPOUND METABOLIC PROCESS | 52 | 1517 | 1.362e-06 | 5.711e-05 |
112 | POSITIVE REGULATION OF MITOTIC CELL CYCLE | 12 | 123 | 1.441e-06 | 5.916e-05 |
113 | POSITIVE REGULATION OF CELLULAR COMPONENT ORGANIZATION | 43 | 1152 | 1.462e-06 | 5.916e-05 |
114 | RESPONSE TO METAL ION | 20 | 333 | 1.454e-06 | 5.916e-05 |
115 | POSITIVE REGULATION OF MULTICELLULAR ORGANISMAL PROCESS | 49 | 1395 | 1.445e-06 | 5.916e-05 |
116 | REGULATION OF MUSCLE TISSUE DEVELOPMENT | 11 | 103 | 1.617e-06 | 6.432e-05 |
117 | REGULATION OF MUSCLE ORGAN DEVELOPMENT | 11 | 103 | 1.617e-06 | 6.432e-05 |
118 | RESPONSE TO STEROID HORMONE | 25 | 497 | 1.868e-06 | 7.365e-05 |
119 | HEAD DEVELOPMENT | 31 | 709 | 2.098e-06 | 8.202e-05 |
120 | SIGNAL TRANSDUCTION BY PROTEIN PHOSPHORYLATION | 22 | 404 | 2.197e-06 | 8.52e-05 |
121 | REGULATION OF CYTOSKELETON ORGANIZATION | 25 | 502 | 2.233e-06 | 8.586e-05 |
122 | CARDIOVASCULAR SYSTEM DEVELOPMENT | 33 | 788 | 2.467e-06 | 9.331e-05 |
123 | CIRCULATORY SYSTEM DEVELOPMENT | 33 | 788 | 2.467e-06 | 9.331e-05 |
124 | POSITIVE REGULATION OF PROTEIN SERINE THREONINE KINASE ACTIVITY | 18 | 289 | 2.944e-06 | 0.0001105 |
125 | POSITIVE REGULATION OF PROTEIN CATABOLIC PROCESS | 17 | 263 | 3.38e-06 | 0.0001254 |
126 | ORGANELLE LOCALIZATION | 22 | 415 | 3.395e-06 | 0.0001254 |
127 | CELLULAR RESPONSE TO EXTERNAL STIMULUS | 17 | 264 | 3.557e-06 | 0.0001296 |
128 | PROTEIN UBIQUITINATION INVOLVED IN UBIQUITIN DEPENDENT PROTEIN CATABOLIC PROCESS | 12 | 134 | 3.566e-06 | 0.0001296 |
129 | PEPTIDYL AMINO ACID MODIFICATION | 34 | 841 | 3.718e-06 | 0.0001341 |
130 | RESPONSE TO TOXIC SUBSTANCE | 16 | 241 | 4.669e-06 | 0.0001671 |
131 | REGULATION OF PROTEIN CATABOLIC PROCESS | 21 | 393 | 5.025e-06 | 0.0001785 |
132 | RESPONSE TO HORMONE | 35 | 893 | 5.251e-06 | 0.0001851 |
133 | EPITHELIAL CELL DIFFERENTIATION | 24 | 495 | 5.634e-06 | 0.0001971 |
134 | REGULATION OF CELLULAR PROTEIN CATABOLIC PROCESS | 17 | 274 | 5.844e-06 | 0.0002029 |
135 | POSITIVE REGULATION OF CELL DIFFERENTIATION | 33 | 823 | 6.18e-06 | 0.000213 |
136 | POSITIVE REGULATION OF CELLULAR PROTEIN CATABOLIC PROCESS | 14 | 192 | 6.32e-06 | 0.0002162 |
137 | HEART DEVELOPMENT | 23 | 466 | 6.629e-06 | 0.0002251 |
138 | NEGATIVE REGULATION OF CHROMOSOME SEGREGATION | 6 | 28 | 6.783e-06 | 0.0002271 |
139 | METAPHASE PLATE CONGRESSION | 7 | 42 | 6.736e-06 | 0.0002271 |
140 | ANAPHASE PROMOTING COMPLEX DEPENDENT CATABOLIC PROCESS | 9 | 77 | 6.846e-06 | 0.0002275 |
141 | CELLULAR RESPONSE TO OXYGEN LEVELS | 12 | 143 | 7.003e-06 | 0.0002311 |
142 | NEGATIVE REGULATION OF CELL PROLIFERATION | 28 | 643 | 7.179e-06 | 0.0002352 |
143 | RESPONSE TO VITAMIN | 10 | 98 | 7.288e-06 | 0.0002371 |
144 | REGULATION OF DNA METABOLIC PROCESS | 19 | 340 | 7.554e-06 | 0.0002441 |
145 | NEGATIVE REGULATION OF PROTEIN COMPLEX DISASSEMBLY | 13 | 170 | 8.09e-06 | 0.0002596 |
146 | INTRACELLULAR SIGNAL TRANSDUCTION | 51 | 1572 | 8.288e-06 | 0.0002641 |
147 | RESPIRATORY SYSTEM DEVELOPMENT | 14 | 197 | 8.492e-06 | 0.0002688 |
148 | DNA INTEGRITY CHECKPOINT | 12 | 146 | 8.667e-06 | 0.0002725 |
149 | RESPONSE TO X RAY | 6 | 30 | 1.039e-05 | 0.0003243 |
150 | CENTROSOME CYCLE | 7 | 45 | 1.084e-05 | 0.0003363 |
151 | POSITIVE REGULATION OF EPITHELIAL CELL MIGRATION | 10 | 103 | 1.138e-05 | 0.0003483 |
152 | REGULATION OF CELLULAR COMPONENT MOVEMENT | 31 | 771 | 1.133e-05 | 0.0003483 |
153 | REGULATION OF OSSIFICATION | 13 | 178 | 1.329e-05 | 0.0004042 |
154 | MITOTIC G2 M TRANSITION CHECKPOINT | 5 | 19 | 1.394e-05 | 0.0004193 |
155 | TISSUE MIGRATION | 9 | 84 | 1.406e-05 | 0.0004193 |
156 | MICROTUBULE ORGANIZING CENTER ORGANIZATION | 9 | 84 | 1.406e-05 | 0.0004193 |
157 | CELL JUNCTION ASSEMBLY | 11 | 129 | 1.451e-05 | 0.0004299 |
158 | POSITIVE REGULATION OF EPITHELIAL CELL PROLIFERATION | 12 | 154 | 1.491e-05 | 0.0004363 |
159 | AMEBOIDAL TYPE CELL MIGRATION | 12 | 154 | 1.491e-05 | 0.0004363 |
160 | CELLULAR RESPONSE TO STRESS | 50 | 1565 | 1.552e-05 | 0.0004514 |
161 | REGULATION OF CARDIAC MUSCLE TISSUE DEVELOPMENT | 7 | 48 | 1.683e-05 | 0.0004833 |
162 | REGULATION OF LIPID KINASE ACTIVITY | 7 | 48 | 1.683e-05 | 0.0004833 |
163 | CELLULAR RESPONSE TO INORGANIC SUBSTANCE | 12 | 156 | 1.698e-05 | 0.0004847 |
164 | ORGANELLE ASSEMBLY | 23 | 495 | 1.747e-05 | 0.0004958 |
165 | POSITIVE REGULATION OF CELL DIVISION | 11 | 132 | 1.803e-05 | 0.0005084 |
166 | G2 DNA DAMAGE CHECKPOINT | 6 | 33 | 1.855e-05 | 0.0005168 |
167 | GLAND DEVELOPMENT | 20 | 395 | 1.848e-05 | 0.0005168 |
168 | NEGATIVE REGULATION OF CELL DEATH | 33 | 872 | 2.015e-05 | 0.0005581 |
169 | LOCOMOTION | 39 | 1114 | 2.045e-05 | 0.0005631 |
170 | PEPTIDYL TYROSINE MODIFICATION | 13 | 186 | 2.123e-05 | 0.0005785 |
171 | POSITIVE REGULATION OF CELL CYCLE PHASE TRANSITION | 8 | 68 | 2.126e-05 | 0.0005785 |
172 | NEGATIVE REGULATION OF MITOTIC NUCLEAR DIVISION | 6 | 34 | 2.22e-05 | 0.000597 |
173 | VISUAL BEHAVIOR | 7 | 50 | 2.217e-05 | 0.000597 |
174 | ANATOMICAL STRUCTURE FORMATION INVOLVED IN MORPHOGENESIS | 35 | 957 | 2.288e-05 | 0.0006117 |
175 | REGENERATION | 12 | 161 | 2.328e-05 | 0.0006191 |
176 | CELLULAR RESPONSE TO EXTRACELLULAR STIMULUS | 13 | 188 | 2.377e-05 | 0.0006226 |
177 | REGULATION OF OSTEOBLAST DIFFERENTIATION | 10 | 112 | 2.382e-05 | 0.0006226 |
178 | NEGATIVE REGULATION OF DEVELOPMENTAL PROCESS | 31 | 801 | 2.372e-05 | 0.0006226 |
179 | NEGATIVE REGULATION OF PROTEIN METABOLIC PROCESS | 38 | 1087 | 2.714e-05 | 0.0007054 |
180 | CELL CYCLE G2 M PHASE TRANSITION | 11 | 138 | 2.735e-05 | 0.0007069 |
181 | POSITIVE REGULATION OF GENE EXPRESSION | 53 | 1733 | 2.784e-05 | 0.0007156 |
182 | RESPONSE TO OXYGEN LEVELS | 17 | 311 | 3.015e-05 | 0.0007688 |
183 | RESPONSE TO LIGHT STIMULUS | 16 | 280 | 3.024e-05 | 0.0007688 |
184 | NEGATIVE REGULATION OF CYTOSKELETON ORGANIZATION | 14 | 221 | 3.091e-05 | 0.0007817 |
185 | NEGATIVE REGULATION OF TRANSCRIPTION FROM RNA POLYMERASE II PROMOTER | 29 | 740 | 3.498e-05 | 0.0008797 |
186 | REGULATION OF CELL ADHESION | 26 | 629 | 3.722e-05 | 0.000931 |
187 | RAS PROTEIN SIGNAL TRANSDUCTION | 11 | 143 | 3.804e-05 | 0.0009465 |
188 | NEGATIVE REGULATION OF CHROMOSOME ORGANIZATION | 9 | 96 | 4.133e-05 | 0.001023 |
189 | EPIDERMAL GROWTH FACTOR RECEPTOR SIGNALING PATHWAY | 7 | 55 | 4.184e-05 | 0.001028 |
190 | POSITIVE REGULATION OF HYDROLASE ACTIVITY | 33 | 905 | 4.197e-05 | 0.001028 |
191 | RESPONSE TO ESTRADIOL | 11 | 146 | 4.605e-05 | 0.001122 |
192 | BIOLOGICAL ADHESION | 36 | 1032 | 4.673e-05 | 0.001133 |
193 | REGULATION OF CELL SUBSTRATE ADHESION | 12 | 173 | 4.731e-05 | 0.001135 |
194 | POSITIVE REGULATION OF MUSCLE TISSUE DEVELOPMENT | 7 | 56 | 4.712e-05 | 0.001135 |
195 | REGULATION OF CELL CYCLE G1 S PHASE TRANSITION | 11 | 147 | 4.902e-05 | 0.001152 |
196 | NEGATIVE REGULATION OF CELL CYCLE G1 S PHASE TRANSITION | 9 | 98 | 4.868e-05 | 0.001152 |
197 | DEVELOPMENTAL PROCESS INVOLVED IN REPRODUCTION | 25 | 602 | 4.878e-05 | 0.001152 |
198 | CENTRAL NERVOUS SYSTEM DEVELOPMENT | 32 | 872 | 4.882e-05 | 0.001152 |
199 | CELLULAR RESPONSE TO NUTRIENT | 6 | 39 | 5.009e-05 | 0.001171 |
200 | REGULATION OF PROTEASOMAL UBIQUITIN DEPENDENT PROTEIN CATABOLIC PROCESS | 11 | 148 | 5.215e-05 | 0.001207 |
201 | DIGESTIVE SYSTEM DEVELOPMENT | 11 | 148 | 5.215e-05 | 0.001207 |
202 | MITOTIC G2 DNA DAMAGE CHECKPOINT | 4 | 13 | 5.439e-05 | 0.001253 |
203 | CELLULAR RESPONSE TO DNA DAMAGE STIMULUS | 28 | 720 | 5.468e-05 | 0.001253 |
204 | REGULATION OF VASCULATURE DEVELOPMENT | 14 | 233 | 5.507e-05 | 0.001256 |
205 | AGING | 15 | 264 | 5.697e-05 | 0.001293 |
206 | INOSITOL LIPID MEDIATED SIGNALING | 10 | 124 | 5.726e-05 | 0.001293 |
207 | NEGATIVE REGULATION OF CELL CYCLE G2 M PHASE TRANSITION | 5 | 25 | 5.853e-05 | 0.001309 |
208 | POSITIVE REGULATION OF CHROMOSOME SEGREGATION | 5 | 25 | 5.853e-05 | 0.001309 |
209 | REPRODUCTION | 42 | 1297 | 5.902e-05 | 0.001314 |
210 | POSITIVE REGULATION OF ORGANELLE ORGANIZATION | 24 | 573 | 6.05e-05 | 0.001334 |
211 | REGULATION OF CELL DEATH | 46 | 1472 | 6.031e-05 | 0.001334 |
212 | POSITIVE REGULATION OF PROTEOLYSIS | 18 | 363 | 6.319e-05 | 0.001387 |
213 | ENZYME LINKED RECEPTOR PROTEIN SIGNALING PATHWAY | 27 | 689 | 6.548e-05 | 0.00143 |
214 | REGULATION OF INTRACELLULAR SIGNAL TRANSDUCTION | 50 | 1656 | 6.692e-05 | 0.001445 |
215 | MITOTIC SPINDLE ASSEMBLY | 6 | 41 | 6.706e-05 | 0.001445 |
216 | MICROTUBULE CYTOSKELETON ORGANIZATION INVOLVED IN MITOSIS | 6 | 41 | 6.706e-05 | 0.001445 |
217 | CELLULAR RESPONSE TO NITROGEN COMPOUND | 22 | 505 | 6.946e-05 | 0.001489 |
218 | NEGATIVE REGULATION OF PROTEIN MODIFICATION PROCESS | 25 | 616 | 7.048e-05 | 0.001504 |
219 | REGULATION OF CATABOLIC PROCESS | 28 | 731 | 7.098e-05 | 0.001508 |
220 | REGULATION OF PROTEIN UBIQUITINATION INVOLVED IN UBIQUITIN DEPENDENT PROTEIN CATABOLIC PROCESS | 9 | 103 | 7.203e-05 | 0.001523 |
221 | STEM CELL PROLIFERATION | 7 | 60 | 7.398e-05 | 0.001558 |
222 | CELLULAR RESPONSE TO VITAMIN D | 4 | 14 | 7.512e-05 | 0.001574 |
223 | DNA GEOMETRIC CHANGE | 8 | 81 | 7.623e-05 | 0.001591 |
224 | POSITIVE REGULATION OF BIOSYNTHETIC PROCESS | 53 | 1805 | 8.167e-05 | 0.001697 |
225 | CELLULAR COMPONENT MORPHOGENESIS | 32 | 900 | 8.83e-05 | 0.001826 |
226 | BRANCHING MORPHOGENESIS OF AN EPITHELIAL TUBE | 10 | 131 | 9.105e-05 | 0.001875 |
227 | REPRODUCTIVE SYSTEM DEVELOPMENT | 19 | 408 | 9.147e-05 | 0.001875 |
228 | REGULATION OF CELLULAR PROTEIN LOCALIZATION | 23 | 552 | 9.309e-05 | 0.0019 |
229 | REGULATION OF CYTOPLASMIC TRANSPORT | 21 | 481 | 9.834e-05 | 0.001998 |
230 | MORPHOGENESIS OF A POLARIZED EPITHELIUM | 5 | 28 | 0.0001038 | 0.002099 |
231 | REGULATION OF GROWTH | 25 | 633 | 0.0001082 | 0.00218 |
232 | RESPONSE TO ESTROGEN | 13 | 218 | 0.0001091 | 0.002188 |
233 | REGULATION OF DNA REPLICATION | 11 | 161 | 0.0001115 | 0.002227 |
234 | LUNG MORPHOGENESIS | 6 | 45 | 0.0001147 | 0.00228 |
235 | POSITIVE REGULATION OF LIGASE ACTIVITY | 9 | 110 | 0.00012 | 0.002375 |
236 | REGULATION OF CARDIAC MUSCLE CELL PROLIFERATION | 5 | 29 | 0.0001236 | 0.002397 |
237 | DNA REPLICATION INITIATION | 5 | 29 | 0.0001236 | 0.002397 |
238 | POSITIVE REGULATION OF CARDIAC MUSCLE TISSUE DEVELOPMENT | 5 | 29 | 0.0001236 | 0.002397 |
239 | RESPONSE TO NUTRIENT | 12 | 191 | 0.0001224 | 0.002397 |
240 | NEUROBLAST PROLIFERATION | 5 | 29 | 0.0001236 | 0.002397 |
241 | NEGATIVE REGULATION OF NUCLEAR DIVISION | 6 | 46 | 0.00013 | 0.002509 |
242 | CELL SUBSTRATE ADHESION | 11 | 164 | 0.0001314 | 0.002511 |
243 | RESPONSE TO ALKALOID | 10 | 137 | 0.0001322 | 0.002511 |
244 | CELLULAR RESPONSE TO RADIATION | 10 | 137 | 0.0001322 | 0.002511 |
245 | DNA METABOLIC PROCESS | 28 | 758 | 0.000131 | 0.002511 |
246 | POSITIVE REGULATION OF HISTONE H3 K4 METHYLATION | 4 | 16 | 0.0001329 | 0.002514 |
247 | SMALL GTPASE MEDIATED SIGNAL TRANSDUCTION | 17 | 352 | 0.0001383 | 0.002604 |
248 | CELLULAR RESPONSE TO LIPID | 20 | 457 | 0.0001392 | 0.002611 |
249 | SMOOTH MUSCLE CELL DIFFERENTIATION | 5 | 30 | 0.0001463 | 0.002734 |
250 | MORPHOGENESIS OF A BRANCHING STRUCTURE | 11 | 167 | 0.0001542 | 0.00287 |
251 | PROTEIN LOCALIZATION | 52 | 1805 | 0.000155 | 0.002873 |
252 | REGULATION OF CELL MATRIX ADHESION | 8 | 90 | 0.0001607 | 0.002967 |
253 | RESPONSE TO CALCIUM ION | 9 | 115 | 0.0001686 | 0.0031 |
254 | RESPONSE TO ACTIVITY | 7 | 69 | 0.0001811 | 0.003317 |
255 | POSITIVE REGULATION OF CATABOLIC PROCESS | 18 | 395 | 0.0001824 | 0.003327 |
256 | REGULATION OF HYDROLASE ACTIVITY | 41 | 1327 | 0.0001993 | 0.003597 |
257 | NEGATIVE REGULATION OF MULTICELLULAR ORGANISMAL PROCESS | 33 | 983 | 0.0001995 | 0.003597 |
258 | CELLULAR RESPONSE TO ABIOTIC STIMULUS | 14 | 263 | 0.0001982 | 0.003597 |
259 | WOUND HEALING | 20 | 470 | 0.0002017 | 0.003609 |
260 | CENTROSOME DUPLICATION | 5 | 32 | 0.000201 | 0.003609 |
261 | REGULATION OF TRANSCRIPTION FROM RNA POLYMERASE II PROMOTER | 51 | 1784 | 0.0002177 | 0.003881 |
262 | UROGENITAL SYSTEM DEVELOPMENT | 15 | 299 | 0.0002256 | 0.004006 |
263 | RESPONSE TO VITAMIN D | 5 | 33 | 0.0002336 | 0.004104 |
264 | POSITIVE REGULATION OF HISTONE METHYLATION | 5 | 33 | 0.0002336 | 0.004104 |
265 | CELL DEVELOPMENT | 43 | 1426 | 0.0002338 | 0.004104 |
266 | MICROTUBULE BASED MOVEMENT | 12 | 205 | 0.0002367 | 0.00414 |
267 | NEGATIVE REGULATION OF GROWTH | 13 | 236 | 0.000239 | 0.004165 |
268 | RESPONSE TO CORTICOSTEROID | 11 | 176 | 0.0002439 | 0.004234 |
269 | RESPONSE TO EXTRACELLULAR STIMULUS | 19 | 441 | 0.0002481 | 0.004291 |
270 | MUSCLE CELL DIFFERENTIATION | 13 | 237 | 0.000249 | 0.004291 |
271 | ASSOCIATIVE LEARNING | 7 | 73 | 0.0002579 | 0.004412 |
272 | G1 DNA DAMAGE CHECKPOINT | 7 | 73 | 0.0002579 | 0.004412 |
273 | GLAND MORPHOGENESIS | 8 | 97 | 0.0002701 | 0.004537 |
274 | ORGAN FORMATION | 5 | 34 | 0.00027 | 0.004537 |
275 | ADHERENS JUNCTION ASSEMBLY | 5 | 34 | 0.00027 | 0.004537 |
276 | REGULATION OF PROTEOLYSIS | 26 | 711 | 0.0002664 | 0.004537 |
277 | CELLULAR RESPONSE TO ALKALOID | 5 | 34 | 0.00027 | 0.004537 |
278 | POSITIVE REGULATION OF CARDIAC MUSCLE CELL PROLIFERATION | 4 | 19 | 0.0002717 | 0.004548 |
279 | POSITIVE REGULATION OF CHROMOSOME ORGANIZATION | 10 | 150 | 0.0002771 | 0.004606 |
280 | REGULATION OF GTPASE ACTIVITY | 25 | 673 | 0.0002763 | 0.004606 |
281 | REGULATION OF CELL DEVELOPMENT | 29 | 836 | 0.0002867 | 0.004747 |
282 | DNA CONFORMATION CHANGE | 14 | 273 | 0.0002904 | 0.004791 |
283 | REGULATION OF ORGAN MORPHOGENESIS | 13 | 242 | 0.0003047 | 0.00501 |
284 | MEIOTIC CELL CYCLE PROCESS | 10 | 152 | 0.0003083 | 0.005051 |
285 | REGULATION OF PROTEASOMAL PROTEIN CATABOLIC PROCESS | 11 | 181 | 0.0003104 | 0.005053 |
286 | RESPONSE TO MINERALOCORTICOID | 5 | 35 | 0.0003106 | 0.005053 |
287 | RESPONSE TO WOUNDING | 22 | 563 | 0.0003232 | 0.005239 |
288 | NEGATIVE REGULATION OF CELL JUNCTION ASSEMBLY | 4 | 20 | 0.0003351 | 0.005395 |
289 | RESPONSE TO UV | 9 | 126 | 0.0003348 | 0.005395 |
290 | POSITIVE REGULATION OF CYTOKINESIS | 5 | 36 | 0.0003557 | 0.005707 |
291 | SKELETAL SYSTEM DEVELOPMENT | 19 | 455 | 0.0003661 | 0.005854 |
292 | CELL JUNCTION ORGANIZATION | 11 | 185 | 0.0003741 | 0.005961 |
293 | BONE DEVELOPMENT | 10 | 156 | 0.0003793 | 0.006024 |
294 | NEGATIVE REGULATION OF CELL DIFFERENTIATION | 23 | 609 | 0.0003838 | 0.006074 |
295 | MEIOTIC CELL CYCLE | 11 | 186 | 0.0003916 | 0.006177 |
296 | TUBE FORMATION | 9 | 129 | 0.0003984 | 0.006262 |
297 | NEGATIVE REGULATION OF TRANSFERASE ACTIVITY | 16 | 351 | 0.0004107 | 0.006434 |
298 | REGULATION OF LIGASE ACTIVITY | 9 | 130 | 0.0004217 | 0.006518 |
299 | ERBB SIGNALING PATHWAY | 7 | 79 | 0.0004203 | 0.006518 |
300 | BONE MORPHOGENESIS | 7 | 79 | 0.0004203 | 0.006518 |
301 | RESPONSE TO PURINE CONTAINING COMPOUND | 10 | 158 | 0.0004197 | 0.006518 |
302 | TRANSMEMBRANE RECEPTOR PROTEIN TYROSINE KINASE SIGNALING PATHWAY | 20 | 498 | 0.0004252 | 0.006551 |
303 | ENDOTHELIAL CELL MIGRATION | 6 | 57 | 0.0004297 | 0.006599 |
304 | CELL MATURATION | 9 | 131 | 0.000446 | 0.006827 |
305 | OOCYTE DIFFERENTIATION | 5 | 38 | 0.0004604 | 0.007024 |
306 | POSITIVE REGULATION OF VASCULATURE DEVELOPMENT | 9 | 133 | 0.0004983 | 0.007577 |
307 | ERBB2 SIGNALING PATHWAY | 5 | 39 | 0.0005208 | 0.007867 |
308 | PROTEIN COMPLEX SUBUNIT ORGANIZATION | 44 | 1527 | 0.0005199 | 0.007867 |
309 | VASCULATURE DEVELOPMENT | 19 | 469 | 0.0005302 | 0.007983 |
310 | DEVELOPMENTAL MATURATION | 11 | 193 | 0.0005347 | 0.008026 |
311 | ORGAN REGENERATION | 7 | 83 | 0.0005678 | 0.008441 |
312 | REGULATION OF MONOOXYGENASE ACTIVITY | 6 | 60 | 0.0005678 | 0.008441 |
313 | POSITIVE REGULATION OF OSTEOBLAST DIFFERENTIATION | 6 | 60 | 0.0005678 | 0.008441 |
314 | LEUKOCYTE MIGRATION | 13 | 259 | 0.0005806 | 0.008603 |
315 | RESPONSE TO CADMIUM ION | 5 | 40 | 0.0005869 | 0.008667 |
316 | ANGIOGENESIS | 14 | 293 | 0.0005886 | 0.008667 |
317 | NEGATIVE REGULATION OF PROTEIN CATABOLIC PROCESS | 8 | 109 | 0.0005944 | 0.008725 |
318 | NEUROGENESIS | 41 | 1402 | 0.0006096 | 0.008864 |
319 | POSITIVE REGULATION OF INTRACELLULAR SIGNAL TRANSDUCTION | 29 | 876 | 0.0006092 | 0.008864 |
320 | POSITIVE REGULATION OF PROTEIN MODIFICATION BY SMALL PROTEIN CONJUGATION OR REMOVAL | 11 | 196 | 0.0006082 | 0.008864 |
321 | REGULATION OF EPITHELIAL CELL MIGRATION | 10 | 166 | 0.0006185 | 0.008965 |
322 | CELLULAR RESPONSE TO HORMONE STIMULUS | 21 | 552 | 0.0006224 | 0.008994 |
323 | REGULATION OF CELLULAR RESPONSE TO GROWTH FACTOR STIMULUS | 12 | 229 | 0.0006422 | 0.009251 |
324 | EMBRYO DEVELOPMENT ENDING IN BIRTH OR EGG HATCHING | 21 | 554 | 0.0006519 | 0.009362 |
325 | BLOOD VESSEL ENDOTHELIAL CELL MIGRATION | 4 | 24 | 0.0006961 | 0.009966 |
Num | GO | Overlap | Size | P Value | Adj. P Value |
---|---|---|---|---|---|
1 | KINASE BINDING | 37 | 606 | 2.6e-11 | 2.416e-08 |
2 | ENZYME BINDING | 67 | 1737 | 2.413e-10 | 1.121e-07 |
3 | PROTEIN KINASE ACTIVITY | 36 | 640 | 4.725e-10 | 1.463e-07 |
4 | PROTEIN COMPLEX BINDING | 43 | 935 | 4.36e-09 | 1.013e-06 |
5 | KINASE ACTIVITY | 40 | 842 | 6.468e-09 | 1.057e-06 |
6 | MACROMOLECULAR COMPLEX BINDING | 55 | 1399 | 6.828e-09 | 1.057e-06 |
7 | RIBONUCLEOTIDE BINDING | 66 | 1860 | 9.968e-09 | 1.323e-06 |
8 | CYTOSKELETAL PROTEIN BINDING | 37 | 819 | 9.015e-08 | 1.025e-05 |
9 | ADENYL NUCLEOTIDE BINDING | 55 | 1514 | 9.927e-08 | 1.025e-05 |
10 | PROTEIN SERINE THREONINE KINASE ACTIVITY | 25 | 445 | 2.465e-07 | 2.29e-05 |
11 | MICROTUBULE BINDING | 16 | 201 | 4.289e-07 | 3.622e-05 |
12 | TRANSFERASE ACTIVITY TRANSFERRING PHOSPHORUS CONTAINING GROUPS | 40 | 992 | 5.186e-07 | 4.015e-05 |
13 | TUBULIN BINDING | 17 | 273 | 5.567e-06 | 0.0003978 |
14 | PROTEIN TYROSINE KINASE ACTIVITY | 13 | 176 | 1.177e-05 | 0.0007812 |
15 | RECEPTOR SIGNALING PROTEIN ACTIVITY | 12 | 172 | 4.47e-05 | 0.002769 |
16 | TRANSMEMBRANE RECEPTOR PROTEIN KINASE ACTIVITY | 8 | 81 | 7.623e-05 | 0.004426 |
17 | CYCLIN DEPENDENT PROTEIN SERINE THREONINE KINASE REGULATOR ACTIVITY | 5 | 28 | 0.0001038 | 0.005671 |
18 | TRANSFORMING GROWTH FACTOR BETA BINDING | 4 | 16 | 0.0001329 | 0.00686 |
19 | CYTOKINE BINDING | 8 | 92 | 0.0001873 | 0.008702 |
20 | RECEPTOR SIGNALING PROTEIN SERINE THREONINE KINASE ACTIVITY | 8 | 92 | 0.0001873 | 0.008702 |
21 | PHOSPHATIDYLINOSITOL 3 KINASE ACTIVITY | 7 | 70 | 0.0001983 | 0.008772 |
Num | GO | Overlap | Size | P Value | Adj. P Value |
---|---|---|---|---|---|
1 | MICROTUBULE CYTOSKELETON | 58 | 1068 | 5.148e-15 | 1.503e-12 |
2 | SPINDLE | 30 | 289 | 3.193e-15 | 1.503e-12 |
3 | CYTOSKELETAL PART | 63 | 1436 | 4.515e-12 | 8.79e-10 |
4 | CYTOSKELETON | 76 | 1967 | 9.84e-12 | 1.437e-09 |
5 | CHROMOSOMAL REGION | 27 | 330 | 2.304e-11 | 2.691e-09 |
6 | CHROMOSOME | 45 | 880 | 6.198e-11 | 6.033e-09 |
7 | CENTROSOME | 32 | 487 | 9.791e-11 | 8.169e-09 |
8 | CHROMOSOME CENTROMERIC REGION | 19 | 174 | 1.79e-10 | 1.306e-08 |
9 | MICROTUBULE ORGANIZING CENTER | 36 | 623 | 2.266e-10 | 1.471e-08 |
10 | SPINDLE POLE | 16 | 126 | 5.34e-10 | 3.119e-08 |
11 | CELL SUBSTRATE JUNCTION | 27 | 398 | 1.525e-09 | 8.095e-08 |
12 | KINETOCHORE | 15 | 120 | 2.328e-09 | 1.133e-07 |
13 | ANCHORING JUNCTION | 29 | 489 | 7.907e-09 | 3.552e-07 |
14 | SPINDLE MIDZONE | 8 | 27 | 1.179e-08 | 4.919e-07 |
15 | MITOTIC SPINDLE | 10 | 55 | 2.927e-08 | 1.14e-06 |
16 | CONDENSED CHROMOSOME | 17 | 195 | 4.975e-08 | 1.816e-06 |
17 | MIDBODY | 14 | 132 | 6.697e-08 | 2.301e-06 |
18 | MICROTUBULE | 24 | 405 | 1.633e-07 | 5.298e-06 |
19 | CONDENSED CHROMOSOME OUTER KINETOCHORE | 5 | 12 | 1.049e-06 | 3.224e-05 |
20 | CONDENSED CHROMOSOME CENTROMERIC REGION | 11 | 102 | 1.467e-06 | 4.283e-05 |
21 | CELL JUNCTION | 42 | 1151 | 3.466e-06 | 9.639e-05 |
22 | CONDENSED NUCLEAR CHROMOSOME CENTROMERIC REGION | 5 | 18 | 1.042e-05 | 0.0002766 |
23 | CYCLIN DEPENDENT PROTEIN KINASE HOLOENZYME COMPLEX | 6 | 31 | 1.269e-05 | 0.0003223 |
24 | CONDENSED NUCLEAR CHROMOSOME | 9 | 85 | 1.549e-05 | 0.0003618 |
25 | SUPRAMOLECULAR FIBER | 28 | 670 | 1.527e-05 | 0.0003618 |
26 | PROTEIN KINASE COMPLEX | 9 | 90 | 2.464e-05 | 0.0005535 |
27 | CELL DIVISION SITE | 7 | 52 | 2.883e-05 | 0.0006235 |
28 | KINESIN COMPLEX | 7 | 55 | 4.184e-05 | 0.0008705 |
29 | MICROTUBULE ASSOCIATED COMPLEX | 11 | 145 | 4.323e-05 | 0.0008705 |
30 | PERINUCLEAR REGION OF CYTOPLASM | 26 | 642 | 5.228e-05 | 0.0009889 |
31 | CELL SURFACE | 29 | 757 | 5.249e-05 | 0.0009889 |
32 | SPINDLE MICROTUBULE | 7 | 58 | 5.931e-05 | 0.001082 |
33 | NUCLEAR CHROMOSOME | 22 | 523 | 0.0001153 | 0.00204 |
34 | MICROVILLUS MEMBRANE | 4 | 19 | 0.0002717 | 0.004667 |
35 | SYNAPTONEMAL COMPLEX | 5 | 35 | 0.0003106 | 0.005183 |
36 | RUFFLE | 10 | 156 | 0.0003793 | 0.006153 |
37 | RUFFLE MEMBRANE | 7 | 80 | 0.0004539 | 0.007164 |
38 | MEMBRANE MICRODOMAIN | 14 | 288 | 0.0004966 | 0.007632 |
39 | LATERAL ELEMENT | 3 | 10 | 0.0005534 | 0.008286 |
Num | Pathway | Pathview | Overlap | Size | P Value | Adj. P Value |
---|---|---|---|---|---|---|
1 | Cell_cycle_hsa04110 | 26 | 124 | 4.461e-21 | 2.32e-19 | |
2 | Signaling_pathways_regulating_pluripotency_of_stem_cells_hsa04550 | 20 | 139 | 3.28e-13 | 8.529e-12 | |
3 | Cellular_senescence_hsa04218 | 21 | 160 | 5.279e-13 | 9.15e-12 | |
4 | FoxO_signaling_pathway_hsa04068 | 19 | 132 | 1.286e-12 | 1.672e-11 | |
5 | PI3K_Akt_signaling_pathway_hsa04151 | 28 | 352 | 1.891e-11 | 1.967e-10 | |
6 | Wnt_signaling_pathway_hsa04310 | 15 | 146 | 3.488e-08 | 3.023e-07 | |
7 | Focal_adhesion_hsa04510 | 17 | 199 | 6.701e-08 | 4.978e-07 | |
8 | Rap1_signaling_pathway_hsa04015 | 17 | 206 | 1.109e-07 | 7.206e-07 | |
9 | HIF_1_signaling_pathway_hsa04066 | 12 | 100 | 1.499e-07 | 8.659e-07 | |
10 | Hippo_signaling_pathway_hsa04390 | 14 | 154 | 4.582e-07 | 2.383e-06 | |
11 | Regulation_of_actin_cytoskeleton_hsa04810 | 16 | 208 | 6.795e-07 | 3.212e-06 | |
12 | Oocyte_meiosis_hsa04114 | 12 | 124 | 1.571e-06 | 6.81e-06 | |
13 | TGF_beta_signaling_pathway_hsa04350 | 10 | 84 | 1.777e-06 | 7.109e-06 | |
14 | ErbB_signaling_pathway_hsa04012 | 10 | 85 | 1.984e-06 | 7.368e-06 | |
15 | Ras_signaling_pathway_hsa04014 | 16 | 232 | 2.861e-06 | 9.919e-06 | |
16 | MAPK_signaling_pathway_hsa04010 | 18 | 295 | 3.926e-06 | 1.276e-05 | |
17 | p53_signaling_pathway_hsa04115 | 8 | 68 | 2.126e-05 | 6.503e-05 | |
18 | mTOR_signaling_pathway_hsa04150 | 11 | 151 | 6.262e-05 | 0.0001809 | |
19 | Jak_STAT_signaling_pathway_hsa04630 | 11 | 162 | 0.0001178 | 0.0003225 | |
20 | Apoptosis_hsa04210 | 10 | 138 | 0.0001404 | 0.000365 | |
21 | Sphingolipid_signaling_pathway_hsa04071 | 9 | 118 | 0.0002049 | 0.0005074 | |
22 | AMPK_signaling_pathway_hsa04152 | 9 | 121 | 0.0002475 | 0.0005851 | |
23 | Hedgehog_signaling_pathway_hsa04340 | 5 | 47 | 0.00124 | 0.002804 | |
24 | Autophagy_animal_hsa04140 | 8 | 128 | 0.00169 | 0.003661 | |
25 | TNF_signaling_pathway_hsa04668 | 7 | 108 | 0.00265 | 0.005511 | |
26 | NF_kappa_B_signaling_pathway_hsa04064 | 6 | 95 | 0.005979 | 0.01196 | |
27 | Adherens_junction_hsa04520 | 5 | 72 | 0.007988 | 0.01538 | |
28 | Gap_junction_hsa04540 | 5 | 88 | 0.01794 | 0.03332 | |
29 | VEGF_signaling_pathway_hsa04370 | 4 | 59 | 0.01865 | 0.03344 | |
30 | cAMP_signaling_pathway_hsa04024 | 8 | 198 | 0.02158 | 0.03741 | |
31 | Phosphatidylinositol_signaling_system_hsa04070 | 5 | 99 | 0.02817 | 0.04726 | |
32 | Ferroptosis_hsa04216 | 3 | 40 | 0.03119 | 0.05068 | |
33 | Phospholipase_D_signaling_pathway_hsa04072 | 6 | 146 | 0.04071 | 0.06415 | |
34 | Cytokine_cytokine_receptor_interaction_hsa04060 | 9 | 270 | 0.04465 | 0.06829 | |
35 | Endocytosis_hsa04144 | 8 | 244 | 0.06089 | 0.09047 | |
36 | Apelin_signaling_pathway_hsa04371 | 5 | 137 | 0.08805 | 0.1272 | |
37 | Mitophagy_animal_hsa04137 | 3 | 65 | 0.1014 | 0.1425 | |
38 | Apoptosis_multiple_species_hsa04215 | 2 | 33 | 0.11 | 0.1505 | |
39 | cGMP_PKG_signaling_pathway_hsa04022 | 5 | 163 | 0.1505 | 0.2006 | |
40 | ECM_receptor_interaction_hsa04512 | 3 | 82 | 0.1675 | 0.2154 | |
41 | Tight_junction_hsa04530 | 5 | 170 | 0.1698 | 0.2154 | |
42 | Phagosome_hsa04145 | 4 | 152 | 0.2661 | 0.3294 | |
43 | Lysosome_hsa04142 | 3 | 123 | 0.3549 | 0.4292 | |
44 | Calcium_signaling_pathway_hsa04020 | 4 | 182 | 0.3823 | 0.4518 | |
45 | Cell_adhesion_molecules_.CAMs._hsa04514 | 3 | 145 | 0.4562 | 0.5157 | |
46 | Necroptosis_hsa04217 | 3 | 164 | 0.538 | 0.5952 |