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EGFR enhances Survivin expression through the phosphoinositide 3 (PI-3) kinase signaling pathway

Qiang Wang1, Mark I Greene

  • 1Department of Pathology and Laboratory Medicine, Abramson Family Cancer Research Institute, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.

Experimental and Molecular Pathology
|June 25, 2005
PubMed

Insights

Epidermal Growth Factor Receptor (EGFR) activation increases Survivin, an apoptosis inhibitor, via the PI-3 kinase pathway. This suggests EGFR contributes to cancer by affecting mitosis and chromosome stability.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • The ErbB receptor tyrosine kinase family, including EGFR, is frequently dysregulated in cancers.
  • ErbB signaling promotes cancer cell proliferation (MAP kinase pathway) and survival (PI-3 kinase pathway).
  • Targeting ErbB receptors can re-sensitize resistant cancer cells to apoptosis.

Purpose of the Study:

  • To investigate the role of activated EGFR in regulating Survivin expression.
  • To determine the signaling pathways mediating EGFR-induced Survivin upregulation.
  • To explore the implications of EGFR-Survivin interaction in cancer development.

Main Methods:

  • Utilized cell culture models with activated and inactivated EGFR.
  • Assessed Survivin mRNA and protein levels using molecular biology techniques.
  • Employed specific pathway inhibitors (PI-3 kinase and MAP kinase inhibitors).

Main Results:

  • Activated EGFR significantly increased Survivin levels (mRNA and protein).
  • EGFR-mediated Survivin upregulation was dependent on the PI-3 kinase pathway.
  • Inhibition of PI-3 kinase abolished EGFR-induced Survivin expression.
  • MAP kinase pathway was not involved in EGFR-driven Survivin regulation.

Conclusions:

  • EGFR activation promotes cancer cell survival by upregulating Survivin through the PI-3 kinase pathway.
  • EGFR may contribute to malignant transformation by impacting mitotic control and chromosome instability via Survivin.
  • Targeting the EGFR-PI-3K-Survivin axis could be a therapeutic strategy for cancers overexpressing EGFR.

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