Altered expression of the catenin p120 in human cancer: implications for tumor progression

Differentiation. 2002 Dec;70(9-10):583-9. doi: 10.1046/j.1432-0436.2002.700911.x.

Abstract

Tumor progression in epithelial tissues is characterized by a series of genetic and epigenetic changes that lead ultimately to metastasis. Alterations in E-cadherin and its cytoplasmic regulators, the catenins, have been implicated as central to this process. Here, we focus on p120-catenin and its rising incidence in the pathology literature as a molecule altered in human tumors. The data show that p120 is frequently altered and/or lost in tumors of the colon, bladder, stomach, breast, prostate, lung, and pancreas. Moreover, in some cases p120 loss appears to be an early event in tumor progression, possibly preceding loss of E-cadherin. Potential roles of p120 as a tumor suppressor or metastasis promoter are discussed.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Catenins
  • Cell Adhesion Molecules / biosynthesis
  • Cell Adhesion Molecules / genetics*
  • Cell Adhesion Molecules / metabolism
  • Female
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Male
  • Neoplasm Metastasis
  • Neoplasms / genetics*
  • Neoplasms / metabolism
  • Neoplasms / pathology*
  • Phosphoproteins / biosynthesis
  • Phosphoproteins / genetics*
  • Phosphoproteins / metabolism

Substances

  • Catenins
  • Cell Adhesion Molecules
  • Phosphoproteins
  • delta catenin