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A nucleotide excision repair master-switch: p53 regulated coordinate induction of global genomic repair genes

S A Amundson1, A Patterson, K T Do

  • 1National Institutes of Health, National Cancer Institute, Division of Basic Science, 37 Convent Dr., Bldg. 37, RM. 6144, Bethesda, Maryland 20892, USA. amundson@box-a.nih.gov

Cancer Biology & Therapy
|August 13, 2002
PubMed

Insights

The tumor suppressor gene p53 regulates DNA repair genes like XPC. This study shows wild-type p53 is essential for XPC induction by various DNA-damaging agents.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • DNA Repair Mechanisms

Background:

  • The p53 tumor suppressor is frequently mutated in human cancers.
  • p53 acts as a transcription factor regulating genes involved in cell cycle control, apoptosis, and DNA repair.
  • p53-regulated genes GADD45a and DDB2 are implicated in global genomic repair (GGR), a sub-pathway of nucleotide excision repair (NER).

Purpose of the Study:

  • To investigate the role of wild-type p53 in the induction of the GGR gene XPC.
  • To determine if XPC induction by DNA-damaging agents is p53-dependent.

Main Methods:

  • Exposure of various human cell lines to ionizing radiation, UV radiation, and alkylating agents.
  • Analysis of XPC gene expression levels following DNA damage.
  • Comparison of XPC induction in cells with and without wild-type p53.

Main Results:

  • XPC gene is induced in response to ionizing radiation, UV radiation, and alkylating agents.
  • This induction of XPC requires the presence of wild-type p53.
  • The findings extend the role of p53 in DNA repair beyond GADD45a and DDB2.

Conclusions:

  • Wild-type p53 is a critical regulator for the induction of the GGR gene XPC.
  • p53-mediated induction of XPC is a key component of the cellular response to diverse DNA-damaging agents.
  • This highlights a broader role for p53 in coordinating DNA repair pathways.

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