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Identification of c-MYC as a target of the APC pathway.

Science (New York, N.Y.) | Sep 4, 1998

http://www.ncbi.nlm.nih.gov/pubmed/9727977

The adenomatous polyposis coli gene (APC) is a tumor suppressor gene that is inactivated in most colorectal cancers. Mutations of APC cause aberrant accumulation of beta-catenin, which then binds T cell factor-4 (Tcf-4), causing increased transcriptional activation of unknown genes. Here, the c-MYC oncogene is identified as a target gene in this signaling pathway. Expression of c-MYC was shown to be repressed by wild-type APC and activated by beta-catenin, and these effects were mediated through Tcf-4 binding sites in the c-MYC promoter. These results provide a molecular framework for understanding the previously enigmatic overexpression of c-MYC in colorectal cancers.

Pubmed ID: 9727977 RIS Download

Mesh terms: Adenomatous Polyposis Coli Protein | Binding Sites | Cell Line | Colorectal Neoplasms | Cytoskeletal Proteins | Gene Expression Regulation, Neoplastic | Genes, APC | Genes, Reporter | Genes, myc | HT29 Cells | Humans | Mutation | Promoter Regions, Genetic | Proto-Oncogene Proteins c-myc | Signal Transduction | TCF Transcription Factors | Trans-Activators | Transcription Factor 7-Like 2 Protein | Transcription Factors | Transcription, Genetic | beta Catenin

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Associated grants

  • Agency: NCI NIH HHS, Id: CA57345
  • Agency: NCI NIH HHS, Id: CA62924
  • Agency: NIGMS NIH HHS, Id: GM07309

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