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DNA damage induces transcriptional activation of p73 by removing C-EBPalpha repression on E2F1

Mirko Marabese1, Faina Vikhanskaya, Cristina Rainelli

  • 1Laboratory of Molecular Pharmacology, Istituto di Ricerche Farmacologiche Mario Negri, via Eritrea 62, 20157 Milan, Italy.

Nucleic Acids Research
|November 7, 2003
PubMed

Insights

DNA damage activates p73 (a p53 family member) by disrupting a repressor complex. This involves the nuclear export of C-EBPalpha, relieving repression on E2F1 and leading to p73 induction in cancer cells.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cellular Signaling

Background:

  • p73, a p53 family protein, is overexpressed in human cancers.
  • p73 regulation differs from p53, especially after DNA damage.

Purpose of the Study:

  • Investigate the mechanism of p73 induction following DNA damage.
  • Identify regulatory factors involved in p73 gene transcription.

Main Methods:

  • Analysis of p73 promoter fragments.
  • Studying protein and mRNA levels post-DNA damage.
  • Investigating transcription factor nuclear localization and DNA binding.

Main Results:

  • DNA damage induces p73 protein and mRNA.
  • E2F1 mediates p73 transcription.
  • C-EBPalpha nuclear export upon DNA damage is crucial for p73 activation.
  • C-EBPalpha represses E2F1 activity by binding to DNA.

Conclusions:

  • A repressor complex including C-EBPalpha and E2F1 normally silences the p73 promoter.
  • DNA damage triggers p73 induction via C-EBPalpha nuclear export and subsequent relief of repression.

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