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Requirement for Akt-mediated survival in cell transformation by the dbl oncogene

S Morley1, J Wagner, K Kauppinen

  • 1Division of Nutritional Sciences, Cornell University, Ithaca, NY 14853, USA.

Cellular Signalling
|August 19, 2006
PubMed

Insights

The Dbl oncogene activates cell proliferation signals. This study reveals Dbl utilizes PI3-kinase/Akt pathways to inhibit apoptosis, promoting cell transformation.

Area of Science:

  • Oncogenic signaling pathways
  • Cellular transformation mechanisms
  • Signal transduction in cancer

Background:

  • The Dbl oncogene activates Cdc42, Rac, and Rho GTPases, transducing proliferative signals.
  • Mechanisms integrating Dbl-induced signals and their role in cell transformation are unclear.
  • The involvement of PI3-kinase and Akt in Dbl-mediated transformation requires investigation.

Purpose of the Study:

  • To investigate the role of PI3-kinase and Akt in Dbl-induced cell transformation.
  • To elucidate the signaling pathways linking Dbl to cell survival and proliferation.
  • To identify novel survival complexes formed downstream of Dbl signaling.

Main Methods:

  • Investigated Akt phosphorylation at threonine 308 in Dbl-expressing cells.
  • Utilized pharmacological and biochemical methods to interfere with the PI3-kinase/Akt pathway.
  • Examined the interaction between activated Cdc42 and PDK1.
  • Assessed apoptosis levels and Bad phosphorylation in response to Dbl expression.

Main Results:

  • Dbl induced PI3-kinase-dependent Akt phosphorylation via Rac and Cdc42.
  • Inhibition of this pathway markedly reduced Dbl-induced focus formation.
  • Dbl expression decreased apoptosis and increased Bad phosphorylation.
  • Activated Cdc42 formed complexes with PDK1, a PI3-kinase effector.

Conclusions:

  • Dbl signaling activates the PI3-kinase/Akt pathway, contributing to cell transformation.
  • This pathway generates anti-apoptotic signals, promoting cell survival.
  • Dbl signaling facilitates the formation of a novel survival complex involving Cdc42 and PDK1.

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