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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

(Download full result)

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
NumGOOverlapSizeP ValueAdj. 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
NumGOOverlapSizeP ValueAdj. 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
NumGOOverlapSizeP ValueAdj. 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

Over-represented Pathway

NumPathwayPathviewOverlapSizeP ValueAdj. 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

Quest ID: 31395e8bf51ef6a3c482c16f1657194b