About Enhancer

Enhancer ID: E_01_0539
Species: human
Position : chr7:79765210-79767210
Biosample name:
Experiment class : High+Lowthroughput
Enhancer type: Enhancer
Disease: Serous ovarian cancer (soc)
Pubmed ID:  29693178
Enhancer experiment: Gene Ontology (GO) analysis,Immunohistochemistry (IHC) analysis,Kaplan?Meier survival analysis,Protein?protein interaction (PPI) network,
Enhancer experiment description: Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non?structural maintenance of chromosomes (non?SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.

About Target gene

Target gene : NCAPH,AURKA
Strong evidence: qRT-PCR,qPCR,ChIP,3C
Less strong evidence: RNA-Seq
Target gene experiment description: Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non?structural maintenance of chromosomes (non?SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.;Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non?structural maintenance of chromosomes (non?SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.;Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non?structural maintenance of chromosomes (non?SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.;Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non?structural maintenance of chromosomes (non?SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.;Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non?structural maintenance of chromosomes (non?SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.

About TF

TF name : GNAI1MMP9EZH2(ENX-1,ENX1b,KMT6,KMT6A,WVS,WVS2,EZH2)
TF experiment: Gene Ontology (GO) analysis,Immunohistochemistry (IHC) analysis,Kaplan?Meier survival analysis,Protein?protein interaction (PPI) network,
TF experiment description: Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non?structural maintenance of chromosomes (non?SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.;Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non?structural maintenance of chromosomes (non?SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.;Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non?structural maintenance of chromosomes (non?SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.;Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non?structural maintenance of chromosomes (non?SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.;Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non?structural maintenance of chromosomes (non?SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.

About Function

Enhancer function : Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non?structural maintenance of chromosomes (non?SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.
Enhancer function experiment: Immunohistochemical staining
Enhancer function
experiment description:		 Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non?structural maintenance of chromosomes (non?SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.

About SNP

SNP ID: --

Upstream Pathway Annotation of TF

GeneName Pathway Name Source Gene Number
GNAI1 5HT1 type receptor mediated signaling pathway panther 27
GNAI1 Adenylate cyclase inactivation signaling ( GPCR signaling (G alpha i) ) inoh 12
GNAI1 Adenylate cyclase inactivation signaling ( GPCR signaling (pertussis toxin) ) inoh 12
GNAI1 Adenylate cyclase inhibitory pathway reactome 14
GNAI1 ADP signalling through P2Y purinoceptor 12 reactome 22
GNAI1 Adrenaline,noradrenaline inhibits insulin secretion reactome 28
GNAI1 Cooperation of PDCL (PhLP1) and TRiC/CCT in G-protein beta folding reactome 42
GNAI1 CXCR3-mediated signaling events pid 38
GNAI1 CXCR4-mediated signaling events pid 87
GNAI1 Endogenous_cannabinoid_signaling panther 23
GNAI1 Endothelins pid 64
GNAI1 Enkephalin release panther 17
GNAI1 G-protein activation reactome 28
GNAI1 G alpha (i) signalling events reactome 241
GNAI1 G alpha (s) signalling events reactome 142
GNAI1 G alpha (z) signalling events reactome 46
GNAI1 G alpha i GDP-GTP exchange signaling ( GPCR signaling (G alpha i) ) inoh 36
GNAI1 G alpha i GDP-GTP exchange signaling ( GPCR signaling (pertussis toxin) ) inoh 36
GNAI1 GABA-B_receptor_II_signaling panther 35
GNAI1 Hedgehog signaling events mediated by Gli proteins pid 49
GNAI1 Heterotrimeric G-protein signaling pathway-Gi alpha and Gs alpha mediated pathway panther 126
GNAI1 Heterotrimeric GPCR signaling pathway (through G alpha i and pertussis toxin) ( GPCR signaling (pertussis toxin) ) inoh 228
GNAI1 Heterotrimeric GTP-binding protein coupled receptor signaling pathway (through G alpha i, adenylate cyclase and cAMP) ( GPCR signaling (G alpha i) ) inoh 228
GNAI1 Inflammation mediated by chemokine and cytokine signaling pathway panther 189
GNAI1 LPA receptor mediated events pid 65
GNAI1 Metabotropic glutamate receptor group II pathway panther 29
GNAI1 Metabotropic glutamate receptor group III pathway panther 54
GNAI1 Muscarinic acetylcholine receptor 2 and 4 signaling pathway panther 38
GNAI1 Negative regulation of (G alpha i GDP-GTP exchange signaling) ( GPCR signaling (G alpha i) ) inoh 21
GNAI1 Negative regulation of (G alpha i GDP-GTP exchange signaling) ( GPCR signaling (pertussis toxin) ) inoh 21
GNAI1 Negative regulation of heterotrimeric GPCR signaling pathway (through G alpha s) ( GPCR signaling (cholera toxin) ) inoh 12
GNAI1 Negative regulation of heterotrimeric GPCR signaling pathway (through G alpha s) ( GPCR signaling (G alpha s, Epac and ERK) ) inoh 12
GNAI1 Nicotine pharmacodynamics pathway panther 28
GNAI1 Nongenotropic Androgen signaling pid 31
GNAI1 Opioid proenkephalin pathway panther 16
GNAI1 Opioid proopiomelanocortin pathway panther 16
GNAI1 PAR1-mediated thrombin signaling events pid 43
GNAI1 Plasma membrane estrogen receptor signaling pid 42
GNAI1 PLC beta mediated events reactome 16
GNAI1 PNAT panther 52
GNAI1 Regulation of insulin secretion reactome 33
GNAI1 S1P1 pathway pid 20
GNAI1 S1P2 pathway pid 26
GNAI1 S1P3 pathway pid 25
GNAI1 S1P4 pathway pid 14
GNAI1 S1P5 pathway pid 8
GNAI1 SHP2 signaling pid 60
GNAI1 Sphingosine 1-phosphate (S1P) pathway pid 21
GNAI1 TSH netpath 82
GNAI1 Chemokine signaling pathway kegg 187
GNAI1 Axon guidance kegg 126
GNAI1 Tight junction kegg 131
GNAI1 Gap junction kegg 87
GNAI1 Leukocyte transendothelial migration kegg 116
GNAI1 Long-term depression kegg 67
GNAI1 Progesterone-mediated oocyte maturation kegg 84
GNAI1 Melanogenesis kegg 100
GNAI1 Gastric acid secretion kegg 68
GNAI1 Chagas disease kegg 103
GNAI1 Toxoplasmosis kegg 131
GNAI1 Hs_Common_Pathways_Underlying_Drug_Addiction_WP2636_89423 wikipathways 9
GNAI1 Hs_Nicotine_Activity_on_Dopaminergic_Neurons_WP1602_78486 wikipathways 8
MMP9 Activation of Matrix Metalloproteinases reactome 32
MMP9 Alzheimer disease-presenilin pathway panther 98
MMP9 amb2 Integrin signaling pid 32
MMP9 AP-1 transcription factor network pid 71
MMP9 Assembly of collagen fibrils and other multimeric structures reactome 44
MMP9 Collagen degradation reactome 39
MMP9 CXCR4-mediated signaling events pid 87
MMP9 Degradation of the extracellular matrix reactome 72
MMP9 EPH-ephrin mediated repulsion of cells reactome 48
MMP9 FGF signaling pathway pid 55
MMP9 LPA receptor mediated events pid 65
MMP9 Osteopontin-mediated events pid 32
MMP9 Plasma membrane estrogen receptor signaling pid 42
MMP9 Plasminogen activating cascade panther 16
MMP9 Regulation of nuclear beta catenin signaling and target gene transcription pid 80
MMP9 Signaling by SCF-KIT reactome 37
MMP9 Syndecan-1-mediated signaling events pid 42
MMP9 Syndecan-4-mediated signaling events pid 32
MMP9 Urokinase-type plasminogen activator (uPA) and uPAR-mediated signaling pid 42
MMP9 Validated targets of C-MYC transcriptional activation pid 80
MMP9 Validated transcriptional targets of AP1 family members Fra1 and Fra2 pid 37
MMP9 Leukocyte transendothelial migration kegg 116
MMP9 Pathways in cancer kegg 321
MMP9 Bladder cancer kegg 38
MMP9 Hs_Angiogenesis_WP1539_88983 wikipathways 17
MMP9 Hs_TNF_related_weak_inducer_of_apoptosis_(TWEAK)_Signaling_Pathway_WP2036_89910 wikipathways 27
EZH2 Activation of anterior HOX genes in hindbrain development during early embryogenesis reactome 120
EZH2 Oxidative Stress Induced Senescence reactome 120
EZH2 PKMTs methylate histone lysines reactome 64
EZH2 PRC2 methylates histones and DNA reactome 71
EZH2 Hs_Endoderm_Differentiation_WP2853_88152 wikipathways 62
EZH2 Hs_Interactome_of_polycomb_repressive_complex_2_(PRC2)_WP2916_88672 wikipathways 15

Enhancer associated network

The number on yellow line represents the distance between enhancer and target gene

Expression of target genes for the enhancer

Enhancer associated SNPs