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Polycomb protein EZH2 regulates E2F1-dependent apoptosis through epigenetically modulating Bim expression.

Z L Wu1, S S Zheng, Z M Li

  • 1Genome Institute of Singapore, Biopolis, Singapore.

Cell Death and Differentiation
|November 7, 2009
PubMed
Summary
This summary is machine-generated.

Cancer cells evade apoptosis through a mechanism involving EZH2, a target of E2F1. EZH2 inhibits the pro-apoptotic protein Bim, allowing tumor cells with aberrant E2F1 activity to survive.

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Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Epigenetics

Background:

  • The pRB/E2F pathway is frequently deregulated in human cancers, impacting cell proliferation and apoptosis.
  • While E2F1's role in apoptosis is known, its regulation in cancer remains unclear.

Purpose of the Study:

  • To investigate the role of EZH2 in regulating E2F1-dependent apoptosis in cancer.
  • To elucidate the mechanism by which cancer cells evade apoptosis despite aberrant E2F1 activity.

Main Methods:

  • RNA interference (RNAi) to deplete EZH2.
  • Analysis of EZH2 and Bim expression.
  • Assessment of E2F1-dependent apoptosis.

Main Results:

  • E2F1 induces the expression of EZH2, an oncogenic histone methyltransferase.
  • EZH2 antagonizes the induction of the pro-apoptotic target Bim by E2F1.
  • Depletion of EZH2 enhances E2F1-dependent Bim expression and promotes apoptosis.

Conclusions:

  • EZH2 acts as a crucial regulator of E2F1-mediated apoptosis.
  • The E2F1-induced expression of EZH2 and Bim creates a fail-safe mechanism for tumor cells to evade apoptosis.
  • This study reveals a novel mechanism of apoptotic restraint in cancer and establishes EZH2's direct role in regulating apoptosis.