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

abstract

  • 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.

published proceedings

  • J Cell Biol

altmetric score

  • 3

author list (cited authors)

  • Murray, N. R., Davidson, L. A., Chapkin, R. S., Clay Gustafson, W., Schattenberg, D. G., & Fields, A. P.

citation count

  • 155

complete list of authors

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

publication date

  • May 1999