Altered SK3/KCa2.3-mediated migration in adenomatous polyposis coli (Apc) mutated mouse colon epithelial cells

Biochem Biophys Res Commun. 2010 Jun 18;397(1):42-7. doi: 10.1016/j.bbrc.2010.05.046. Epub 2010 May 26.

Abstract

Lost of adenomatous polyposis coli gene (Apc) disturbs the migration of intestinal epithelial cells but the mechanisms have not been fully characterized. Since we have demonstrated that SK3/KCa2.3 channel promotes cancer cell migration, we hypothesized that Apc mutation may affect SK3/KCa2.3 channel-mediated colon epithelial cell motility. We report evidence that SK3/KCa2.3 channel promotes colon epithelial cells motility. Following Apc mutation SK3/KCa2.3 expression is largely reduced leading to a suppression of the SK3/KCa2.3 channel mediated-cell migration. Our findings reveal a previously unknown function of the SK3/KCa2.3 channel in epithelial colonic cells, and suggest that Apc is a powerful regulator SK3/KCa2.3 channel.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenomatous Polyposis Coli Protein / genetics
  • Adenomatous Polyposis Coli Protein / metabolism*
  • Animals
  • Cell Line
  • Cell Movement*
  • Colon / cytology
  • Colon / metabolism*
  • Intestinal Mucosa / cytology
  • Intestinal Mucosa / metabolism
  • Mice
  • Mice, Mutant Strains
  • Small-Conductance Calcium-Activated Potassium Channels

Substances

  • Adenomatous Polyposis Coli Protein
  • Kcnn3 protein, mouse
  • Small-Conductance Calcium-Activated Potassium Channels