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Overexpression of protein kinase C betaII induces colonic hyperproliferation and increased sensitivity to colon carcinogenesis.

Protein kinase C betaII (PKC betaII) has been implicated in proliferation of the intestinal epithelium. To investigate PKC betaII function in vivo, we generated transgenic mice that overexpress PKC betaII in the intestinal epithelium. Transgenic PKC betaII mice exhibit hyperproliferation of the colonic epithelium and an increased susceptibility to azoxymethane-induced aberrant crypt foci, preneoplastic lesions in the colon. Furthermore, transgenic PKC betaII mice exhibit elevated colonic beta-catenin levels and decreased glycogen synthase kinase 3beta activity, indicating that PKC betaII stimulates the Wnt/adenomatous polyposis coli (APC)/beta-catenin proliferative signaling pathway in vivo. These data demonstrate a direct role for PKC betaII in colonic epithelial cell proliferation and colon carcinogenesis, possibly through activation of the APC/beta-catenin signaling pathway.

Pubmed ID: 10330400


  • Murray NR
  • Davidson LA
  • Chapkin RS
  • Clay Gustafson W
  • Schattenberg DG
  • Fields AP


The Journal of cell biology

Publication Data

May 17, 1999

Associated Grants

  • Agency: NCI NIH HHS, Id: CA59034
  • Agency: NCI NIH HHS, Id: CA81436

Mesh Terms

  • Animals
  • Colon
  • Colonic Neoplasms
  • Cytoskeletal Proteins
  • Gene Expression
  • Intestinal Mucosa
  • Isoenzymes
  • Mice
  • Mice, Inbred C3H
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Protein Kinase C
  • Protein Kinase C beta
  • Signal Transduction
  • Trans-Activators
  • beta Catenin