Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

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


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


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