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Deregulated transcription factor E2F-1 expression leads to S-phase entry and p53-mediated apoptosis

X Q Qin1, D M Livingston, W G Kaelin

  • 1Division of Neoplastic Disease Mechanisms, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115.

Proceedings of the National Academy of Sciences of the United States of America
|November 8, 1994
PubMed

Insights

The transcription factor E2F-1 induces cell cycle progression and apoptosis. Wild-type RB or a dominant-negative p53 mutant suppressed E2F-1-induced apoptosis, suggesting p53

Area of Science:

  • Molecular Biology
  • Cell Cycle Regulation
  • Apoptosis

Background:

  • E2F-1 is a transcription factor crucial for S phase gene activation.
  • E2F-1 is a known target of the retinoblastoma (RB) gene product.
  • Dysregulation of cell cycle control is implicated in various diseases.

Purpose of the Study:

  • To investigate the role of E2F-1 in cell cycle progression and apoptosis.
  • To determine the involvement of RB and p53 in E2F-1-mediated apoptosis.

Main Methods:

  • Induction of E2F-1 in quiescent fibroblasts.
  • Coexpression of wild-type RB, RB mutants, wild-type p53, or dominant-negative p53 mutants.
  • Assessment of S-phase entry and apoptosis.

Main Results:

  • E2F-1 induction triggered S-phase entry and subsequent apoptosis.
  • Wild-type RB and dominant-negative p53 suppressed E2F-1-induced apoptosis.
  • Loss-of-function RB mutant and wild-type p53 did not suppress apoptosis.

Conclusions:

  • Deregulated E2F-1 activity generates both proliferative and apoptotic signals.
  • p53 plays a role in executing E2F-1-induced apoptosis.
  • RB and p53 function in a pathway that can counteract E2F-1-driven cell death.

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