Growth factor activation of MAP kinase requires cell adhesion

Related Experiment Video

Updated: Oct 31, 2026

Assay for Adhesion and Agar Invasion in S. cerevisiae
04:36

Assay for Adhesion and Agar Invasion in S. cerevisiae

Published on: November 8, 2006

M W Renshaw1, X D Ren, M A Schwartz

  • 1Department of Vascular Biology, The Scripps Research Institute, 10550 N. Torrey Pines Road, La Jolla, CA 92037, USA.

The EMBO Journal
|October 6, 1997
PubMed

Insights

Cell adhesion is crucial for activating the MAP kinase pathway (ERK2) via growth factors. This finding explains how cancer cells achieve anchorage-independent growth.

Area of Science:

  • Cellular biology
  • Molecular biology
  • Cancer research

Background:

  • The MAP kinase pathway regulates normal and oncogenic cell growth.
  • Understanding the regulation of this pathway is key to cancer research.

Purpose of the Study:

  • To investigate the role of cell adhesion in MAP kinase pathway activation.
  • To elucidate the mechanisms underlying anchorage-independent growth in cancer.

Main Methods:

  • Studied ERK2 activation in response to serum and growth factors under varying cell adhesion conditions.
  • Analyzed the activation of Ras, Raf, and MEK proteins in suspended and adherent cells.
  • Investigated the effect of activated MEK on ras-transformed cells in suspension and adherence.

Main Results:

  • ERK2 activation by soluble growth factors requires cell adhesion.
  • Ras and Raf are activated by serum in suspended cells, but MEK activity is inhibited.
  • Activated Ras and Raf still require adhesion for ERK2 activation, while activated MEK does not.
  • Activated MEK promotes growth of ras-transformed cells in suspension.

Conclusions:

  • A novel crosstalk exists between cell adhesion and growth factor signaling pathways.
  • This synergism explains how oncogenic MAP kinase activation leads to both serum- and anchorage-independent growth.

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