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Related Experiment Videos

Raf-MEK-Erk cascade in anoikis is controlled by Rac1 and Cdc42 via Akt.

O Zugasti1, W Rul, P Roux

  • 1Institut de Génétique Moléculaire, CNRS UMR5535, F-34293 Montpellier Cedex 5, France.

Molecular and Cellular Biology
|September 5, 2001
PubMed
Summary

Loss of cell anchorage triggers apoptosis by activating p53 and moderate Erk signaling, involving phosphatidlyinositol 3-kinase and Akt. Rho GTPases control these pathways, crucial for cell death.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Extracellular matrix signals are vital for cell survival.
  • Loss of anchorage can induce apoptosis (anoikis).
  • Rho family GTPases (Rac1, Cdc42) regulate cell survival and death pathways.

Purpose of the Study:

  • To characterize the proapoptotic extracellular signal-regulated kinase (Erk) signal.
  • To elucidate the signaling pathway linking Rho GTPases to anoikis.
  • To identify key molecular components involved in anchorage-loss-induced apoptosis.

Main Methods:

  • Utilized dominant-negative mutants of Rac1 and Cdc42 in primary mouse fibroblasts.
  • Investigated the activation of p53, phosphatidlyinositol 3-kinase (PI3K), Akt, and the Raf-MEK-Erk cascade.

Related Experiment Videos

  • Analyzed the intensity of kinase activation to differentiate survival and death signals.

    • Main Results:

    • Loss of Rac1 and Cdc42 GTP-bound forms induced apoptosis.
    • A proapoptotic, moderate activation of the Raf-MEK-Erk cascade was observed.
    • This Erk activation involved PI3K and Akt signaling.
    • Concomitant activation of p53 and inhibition of Akt were necessary and sufficient for anoikis.

    Conclusions:

    • Rho family GTPases (Rac1, Cdc42) regulate p53, Akt, and Erk signaling pathways.
    • These pathways collaborate to induce apoptosis upon loss of anchorage.
    • The intensity of Erk activation distinguishes survival from apoptotic signaling.