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The involvement of XPC protein in the cisplatin DNA damaging treatment-mediated cellular response

Gan Wang1, Alan Dombkowski, Lynn Chuang

  • 1Institute of Environmental Health Sciences, Wayne State University, 2727 Second Avenue, Detroit, MI 48201, USA. g.wang@wayne.edu

Cell Research
|September 9, 2004
PubMed

Insights

The XPC protein is crucial for cellular response to cisplatin DNA damage, impacting cell cycle and DNA repair genes. XPC deficiency weakens the cellular response, potentially contributing to cancer drug resistance.

Area of Science:

  • Molecular Biology
  • Genetics
  • Cellular Biology

Background:

  • DNA damage recognition is vital for cellular response.
  • XPC protein is a key player in nucleotide excision repair (NER).
  • Cisplatin is a widely used chemotherapy agent that induces DNA damage.

Purpose of the Study:

  • To investigate the role of XPC protein in the cellular response to cisplatin treatment.
  • To identify genes regulated by XPC during cisplatin-induced DNA damage.
  • To elucidate the signaling pathways involving XPC in response to DNA damage.

Main Methods:

  • Microarray analysis to compare gene expression in normal and XPC-defective human fibroblasts after cisplatin treatment.
  • RT-PCR based real-time PCR to validate microarray data.
  • Western blot hybridization to assess caspase-3 activation.
  • Analysis of p53 protein response to cisplatin treatment in the presence and absence of XPC.

Main Results:

  • Microarray analysis identified 861 XPC-responsive genes, with cell cycle and proliferation genes being most affected.
  • RT-PCR confirmed the reliability of microarray data for most tested genes.
  • XPC deficiency significantly attenuated cisplatin-induced caspase-3 activation.
  • XPC defect reduced cisplatin-mediated p53 response.

Conclusions:

  • XPC protein plays a significant role in the cellular response to cisplatin-induced DNA damage.
  • XPC influences cell cycle progression, DNA repair, and signal transduction pathways following DNA damage.
  • The findings suggest a potential mechanism for cancer cell drug resistance related to XPC function.

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