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Molecular Biology and Genetics |
Laboratory of Genetic Instability and Cancer, UPR 2169 CNRS, 94801 Villejuif Cedex, France [F. L. P., A. S.], and Laboratoire de Vectorologie et Transfert de gènes, CNRS UMR #1582 [V. R., D. M., J. C., M. P.] and Laboratoire de Génétique Oncologique, CNRS UMR #1599 [J. F.], Institut Gustave-Roussy, 94805 Villejuif Cedex, France
The breast and ovarian cancer susceptibility genes, BRCA1 and BRCA2, are likely to participate in DNA lesion processing. Oxidative lesions, such as 8-oxoguanine, occur in DNA after endogenous or exogenous oxidative stress. We show that deficiency for either BRCA1 or BRCA2 in human cancer cells leads to a block of the RNA polymerase II transcription machinery at the 8-oxoguanine site and impairs the transcription-coupled repair of the lesion, leading to a high mutation rate. Expression of wild-type BRCA1 from a recombinant adenovirus fully complements the repair defect in BRCA1-deficient cells. These results represent the first demonstration of the essential contribution of BRCA1 and BRCA2 gene products in the repair of the 8-oxoguanine oxidative damage specifically located on the transcribed strand in human cells. This suggests that cells from individuals predisposed to breast and/or ovarian cancer may undergo a high rate of mutations because of the deficiency of this damage repair pathway after oxidative stress.
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