Intercellular junctions: downstream and upstream of Ras?

Semin Cell Dev Biol. 2000 Aug;11(4):309-14. doi: 10.1006/scdb.2000.0181.

Abstract

Most human tumors are of epithelial origin, and these tumors gradually lose their epithelial character in a process termed the epithelial-mesenchymal transition. Approximately 40% of human tumors have activating mutations in one of the three RAS genes. Given these statistics, it is critically important to understand the role of Ras signaling in the epithelial-mesenchymal transition. This review considers the mechanisms and effectors through which Ras may regulate intercellular junction formation in epithelial cells. Conversely, intercellular junction proteins themselves may play a role in regulating Ras activation and signaling.

Publication types

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

MeSH terms

  • Animals
  • Drosophila
  • Epithelial Cells / metabolism
  • Female
  • Gene Expression Regulation, Neoplastic
  • Genes, ras*
  • Humans
  • Intercellular Junctions / metabolism*
  • Kinesins
  • Microfilament Proteins / metabolism
  • Models, Biological
  • Mutation
  • Myosins
  • Neoplasms / genetics
  • Neoplasms / metabolism
  • Retinal Cone Photoreceptor Cells / cytology
  • Retinal Cone Photoreceptor Cells / metabolism
  • Signal Transduction

Substances

  • AFDN protein, human
  • Microfilament Proteins
  • afadin
  • Myosins
  • Kinesins