Cell-adhesion-dependent influences on genomic instability and carcinogenesis

Curr Opin Cell Biol. 1998 Oct;10(5):647-53. doi: 10.1016/s0955-0674(98)80041-0.

Abstract

Adhesion-dependent cell signaling is known to be important in carcinogenesis. It is postulated that several types of adhesion molecules act as tumor suppressor genes by enforcing cell-substrate and cell-cell adhesion thereby preventing the migration of cells and their invasion into surrounding tissues. Recent evidence, however, suggests that disruption of adhesion systems can both initiate neoplastic transformation and contribute a rate-limiting step to progression. Adhesion may modulate neoplastic processes by altering pathways that control genomic stability. Analysis of the adhesion-controlled inactivation of the p53 protein and the concomitant relaxation of cell cycle checkpoint control could identify the critical contributions of adhesion-mediated influences to carcinogenesis.

Publication types

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

MeSH terms

  • Cell Adhesion*
  • Cell Cycle
  • Cell Transformation, Neoplastic / genetics*
  • Cell Transformation, Viral
  • Models, Biological
  • Mutagenesis*
  • Signal Transduction
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Tumor Suppressor Protein p53