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Role for the p53 homologue p73 in E2F-1-induced apoptosis

M Irwin1, M C Marin, A C Phillips

  • 1Dana-Farber Cancer Institute and Brigham and Womens Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.

Nature
|October 18, 2000
PubMed

Insights

The transcription factor E2F-1 triggers cell death through p53-dependent and independent routes. This study reveals E2F-1 activates p73, a p53 homolog, to induce apoptosis even when p53 is absent.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • The transcription factor E2F-1 plays a dual role in cell cycle progression and apoptosis.
  • E2F-1 utilizes both p53-dependent and p53-independent pathways to induce cell death.
  • The p53-dependent pathway involves E2F-1 inducing p14ARF, which neutralizes HDM2 and stabilizes p53.

Purpose of the Study:

  • To investigate the role of the p53 homolog p73 in E2F-1-induced apoptosis.
  • To determine if E2F-1 can induce apoptosis through p73 in the absence of functional p53.

Main Methods:

  • Analysis of E2F-1's effect on p73 transcription.
  • Assessment of E2F-1-induced apoptosis in cells with disrupted p73 function.
  • Experiments conducted in p53-defective tumor cells and p53-/- mouse embryo fibroblasts.

Main Results:

  • E2F-1 was shown to induce the transcription of p73.
  • Disruption of p73 function significantly inhibited E2F-1-induced apoptosis.
  • This inhibition was observed in both p53-defective tumor cells and p53-/- mouse embryo fibroblasts.

Conclusions:

  • Activation of p73 is a mechanism by which E2F-1 can induce apoptosis.
  • E2F-1 can trigger cell death via p73 even in the absence of p53.
  • This finding highlights the importance of the p73 pathway in E2F-1-mediated cellular responses.

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