Name
Caco-2
Annospace Keyword
CellLine
Annospace Name
Experimental Factor Ontology (EFO)
Annospace Version
20170511
Annospace URL
https://arty.scai.fraunhofer.de/artifactory/bel/annotation/cell-line/cell-line-20170511.belanno

Sample Edges 5

p(HGNC:IGF1) increases p(HGNC:CTNNB1)

IGF-1 also enhanced the stability of beta-catenin protein. PubMed:11035789

Annotations
NCBI Taxonomy Ids
9606
Experimental Factor Ontology (EFO)
Caco-2
Experimental Factor Ontology (EFO)
DLD-1 cell
Disease Ontology (DO)
colorectal cancer
MeSH
Plasma

p(HGNC:IGF1) increases act(p(HGNC:CTNNB1), ma(tscript))

To investigate whether IGF-1 also enhanced transactivation potential, a reporter gene assay was performed in HEK293 cells. We used a reporter construct incorporating multimeric Lef/Tcf promoter sequences upstream of a luciferase reporter (TOPFLASH) and a control construct containing mutated promoter sequences (FOPFLASH, ref. 21). We cotransfected TOPFLASH or FOPFLASH, ?-catenin, and human wild-type Tcf-4 wild-type expression constructs into 293 cells. Optimized luciferase assays showed a basal level of TOP/FOP activity of between 4:1 and 20:1. Forty-eight hours after transfection, serum-starved 293 cells were treated with IGF-1 or insulin for 3 or 6 h. These factors alone failed to alter basal reporter activity (Fig. 6 b). A 16-h pretreatment of the transfectants with LiCl had a dramatic effect on reporter activity, with significant enhancement at 50 mM LiCl (P < 0.01 by Tukey's test for comparison with activity in the absence of LiCl). We saw a further increase in reporter activity when we added 50 ng/ml (6.5 nM) IGF-1 to transfectants pretreated with LiCl at 10 mM (P < 0.01 after 6 h of IGF-1 treatment) and at 50 mM (P < 0.01 after 3 h of IGF-1 treatment and P < 0.001 after 6 h). PubMed:11035789

Annotations
NCBI Taxonomy Ids
9606
Experimental Factor Ontology (EFO)
Caco-2
Experimental Factor Ontology (EFO)
DLD-1 cell
Disease Ontology (DO)
colorectal cancer
MeSH
Plasma

p(HGNC:APC) decreases p(HGNC:CTNNB1)

Most colorectal cancers have loss of function mutations in the adenomatosis polyposis coli (APC) tumor suppressor gene. This leads to accumulation of beta-catenin, which together with the DNA binding protein TCF-4 functions as a transcriptional activator. PubMed:10514384

Annotations
NCBI Taxonomy Ids
9606
Experimental Factor Ontology (EFO)
Caco-2
Experimental Factor Ontology (EFO)
DLD-1 cell
Disease Ontology (DO)
colorectal cancer
MeSH
Plasma

complex(p(HGNC:CTNNB1), p(HGNC:TCF4)) increases act(p(HGNC:CTNNB1), ma(tscript))

Here it is shown that one of the target genes of Tcf4 in epithelial cells is Tcf1 (NOTE: TCF7 is the current gene symbol for Tcf1) ....(from full text) ... Tcf1 expression is regulated by APC and beta -catenin-Tcf4. ...We sequenced 1/2 kb directly upstream of promoter I and found the region to be a CpG island containing two potential Tcf0binding motifs (Fig. 2B). The combination of beta -catenin and Tcf4 transactivated the enhancer three- to fourfold in a transient reporter assay (Fig. 2C). Furthermore, expression of a dominant-negative Tcf4 (Delta NTcf4, which lacks the beta -catenin interaction domain) inhibited enhancer activity in LS174T colorectal cancer cells (Fig. 2D). PubMed:10489374

Annotations
NCBI Taxonomy Ids
9606
Experimental Factor Ontology (EFO)
Caco-2
Experimental Factor Ontology (EFO)
DLD-1 cell
Disease Ontology (DO)
colorectal cancer
MeSH
Plasma

complex(p(HGNC:CDH1), p(HGNC:CTNNB1)) decreases bp(GOBP:"cell migration")

IGFs can enhance cell migration, which is known to be influenced via regulation of the E-cadherin/beta-catenin complex. IGF-1 causes tyrosine phosphorylation and stabilization of beta-catenin. These effects may contribute to transformation, cell migration, and a propensity for metastasis in vivo. PubMed:11035789

Annotations
NCBI Taxonomy Ids
9606
Experimental Factor Ontology (EFO)
Caco-2
Experimental Factor Ontology (EFO)
DLD-1 cell
Disease Ontology (DO)
colorectal cancer
MeSH
Plasma

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of the open source project, PyBEL. Please feel free to contact us here to give us feedback or report any issues.