A novel function of CD82/KAI-1 on E-cadherin-mediated homophilic cellular adhesion of cancer cells

Cancer Lett. 2008 Aug 8;266(2):163-70. doi: 10.1016/j.canlet.2008.02.058. Epub 2008 Apr 18.

Abstract

In this study, we analyzed the effect of the metastasis suppressor CD82/KAI-1, a member of the tetraspanin superfamily, on intercellular adhesion on cancer cells. The newly established invasion assay and the cell aggregation assay revealed that CD82 strengthens E-cadherin-mediated intercellular adhesion. Interestingly, ectopic expression of CD82 stabilized E-cadherin/beta-catenin complex formation. Furthermore, CD82 reduced tyrosine phosphorylation of beta-catenin on HGF stimulation. Taken together, CD82 may stabilize or strengthen E-cadherin-dependent intercellular adhesion by regulating beta-catenin-mediated signal transduction on cancer cells, and consequently, prevent cancer cells from seceding from the primary tumor site.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cadherins / metabolism*
  • Cell Adhesion
  • Cell Line, Tumor
  • Cell Movement
  • Humans
  • Kangai-1 Protein / physiology*
  • Neoplasms / metabolism*
  • Neoplasms / pathology
  • Phosphorylation
  • Tyrosine / metabolism
  • beta Catenin / chemistry
  • beta Catenin / metabolism

Substances

  • Cadherins
  • Kangai-1 Protein
  • beta Catenin
  • Tyrosine