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Published online 23 April 2004

Nucleic Acids Research, 2004, Vol. 32, No. 7 2231-2240
© 2004 Oxford University Press

The initiative role of XPC protein in cisplatin DNA damaging treatment-mediated cell cycle regulation

Gan Wang*, Lynn Chuang, Xiaohong Zhang, Stephanie Colton, Alan Dombkowski, John Reiners, Amy Diakiw and Xiaoxin Susan Xu

Institute of Environmental Health Sciences, Wayne State University, 2727 Second Avenue, Room 4325, Detroit, MI 48201, USA

*To whom correspondence should be addressed. Tel: +1 313 964 8140; Fax: +1 313 577 0082; Email: g.wang{at}wayne.edu

Received October 14, 2003; Revised and Accepted March 23, 2004

XPC is an important DNA damage recognition protein involved in DNA nucleotide excision repair. We have studied the role of the XPC protein in cisplatin treatment-mediated cell cycle regulation. Through the comparison of microarray data obtained from human normal fibroblasts and two individual XPC-defective cell lines, 486 genes were identified as XPC-responsive genes in the cisplatin treatment (with a minimal 1.5-fold change) and 297 of these genes were further mapped to biological pathways and gene ontologies. The cell cycle and cell proliferation-related genes were the most affected genes by the XPC defect in the cisplatin treatment. Many other cellular function genes were also affected by the XPC defect in the treatment. Western blot hybridization results revealed that the XPC defect reduced the p53 responses to the cisplatin treatment. The ability to activate caspase-3 was also attenuated in the XPC cells with the treatment. These results suggest that the XPC protein plays a critical role in initiating the cisplatin DNA damaging treatment-mediated signal transduction process, resulting in activation of the p53 pathway and cell cycle arrest that allow DNA repair and apoptosis to take place. These results reveal an important role of the XPC protein in the cancer prevention.


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