XPB is an essential component of the nucleotide excision repair and has been reported by immunoprecipitating studies to associate with p53. The role of the interaction between p53 and XPB in determining cell sensitivity to DNA damaging agents has still to be defined. We have evaluated the effects of XPB overexpression on UV and cisplatin (whose lesions are substrate for nucleotide excision repair pathway) sensitivities in a human ovarian cancer cell line, expressing or not a wild type like p53. XPB overexpression did not change significantly cellular sensitivities to cisplatin and UV treatments, independently of the presence of a wt p53. The overexpression of XPB protein did not result in significant changes in repair activity as demonstrated by the host cell reactivation assay performed in the different cell systems. Moreover the presence of high XPB levels did not change the transactivating activity of wt p53, measured as total cellular levels of p21waf1 after induction of DNA damage.

Keywords: DNA Repair, nucleotide excision repair, Anticancer drugs, DNA Damage, p53