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

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

Authors

  • He TC
  • Sparks AB
  • Rago C
  • Hermeking H
  • Zawel L
  • da Costa LT
  • Morin PJ
  • Vogelstein B
  • Kinzler KW

Journal

Science (New York, N.Y.)

Publication Data

September 4, 1998

Associated Grants

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

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