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DNA damage down-regulates ΔNp63α and induces apoptosis independent of wild type p53

Xiaorong Li1, Jing Chen, Yong Yi

  • 1Center for Growth, Metabolism and Aging, College of Life Sciences, Sichuan University, Chengdu 610064, PR China.

Biochemical and Biophysical Research Communications
|June 5, 2012
PubMed

Insights

DNA damage agents reduce the protein levels of p63 homolog ΔNp63α, promoting apoptosis in cells with mutant p53. This suggests ΔNp63α plays a role in DNA damage-induced cell death.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • The tumor suppressor p53 is crucial for cell cycle arrest and apoptosis in response to DNA damage.
  • p63 proteins, homologs of p53, are increasingly recognized for their roles in apoptosis under specific conditions.

Purpose of the Study:

  • To investigate the role of ΔNp63α in apoptosis induced by DNA damage, particularly in cells with mutant p53.
  • To elucidate the regulatory mechanisms of ΔNp63α expression following DNA damage.

Main Methods:

  • Treatment of FaDu and HaCat cells (carrying mutant p53) with DNA damaging agents.
  • Analysis of ΔNp63α mRNA and protein levels.
  • Knockdown and exogenous expression of ΔNp63α to assess its role in apoptosis and DNA damage sensitivity.

Main Results:

  • DNA damage agents down-regulated ΔNp63α protein levels in FaDu and HaCat cells.
  • DNA damage reduced steady-state mRNA levels of ΔNp63α without significantly affecting protein stability.
  • Knockdown of ΔNp63α induced apoptosis and sensitized cells to DNA damage, while its overexpression conferred resistance.

Conclusions:

  • DNA damage leads to the down-regulation of ΔNp63α.
  • Reduced ΔNp63α levels appear to directly contribute to DNA damage-induced apoptosis.
  • ΔNp63α functions as a modulator of cellular response to DNA damage.

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