Oncogenic c-H-ras deregulates survivin expression: an improvement for survival

FEBS Lett. 2007 Oct 16;581(25):4921-6. doi: 10.1016/j.febslet.2007.09.023. Epub 2007 Sep 21.

Abstract

Survivin protein accomplishes two basic functions: cell cycle regulation and control of apoptosis. It is only expressed in G2/M phase and it influences rescue pathways in apoptosis-induced cells. Overexpression of constitutive active c-H-ras in HeLa, or induction of c-H-ras in a stable HeLaDiR cell line, led to sustained survivin expression in all cell cycle phases and even protected cells from drug induced apoptosis. siRNA-mediated silencing of survivin reversed this protection. Here we link the anti-apoptotic property of survivin to its cell cycle (in)dependent regulation via the activity of oncogenic c-H-ras.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis*
  • Cell Cycle
  • Doxorubicin / antagonists & inhibitors
  • Doxorubicin / toxicity
  • HeLa Cells
  • Humans
  • Inhibitor of Apoptosis Proteins
  • Microtubule-Associated Proteins / antagonists & inhibitors
  • Microtubule-Associated Proteins / metabolism*
  • Neoplasm Proteins / antagonists & inhibitors
  • Neoplasm Proteins / metabolism*
  • Oncogene Protein p21(ras) / metabolism*
  • RNA Interference
  • Survivin

Substances

  • BIRC5 protein, human
  • Inhibitor of Apoptosis Proteins
  • Microtubule-Associated Proteins
  • Neoplasm Proteins
  • Survivin
  • Doxorubicin
  • Oncogene Protein p21(ras)