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[Cancer Research 62, 4899-4902, September 1, 2002]
© 2002 American Association for Cancer Research

Advances in Brief

Transcription-coupled Nucleotide Excision Repair as a Determinant of Cisplatin Sensitivity of Human Cells1

Takahisa Furuta, Takahiro Ueda, Gregory Aune, Alain Sarasin, Kenneth H. Kraemer and Yves Pommier2

Laboratory of Molecular Pharmacology [T. F., G. A., Y. P.], Basic Research Laboratory [T. U., K. H. K.], Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892-4255, and Laboratory of Genetic Instability and Cancer UPR2169 Centre National de la Recherche Scientifique, Institut de Recherches sur le Cancer, 94801 Villejuif, France [A. S.]

The resistance of tumor cells to chemotherapeutic agents, such as cisplatin,is an important problem to be solved in cancer chemotherapy. One of the mechanisms associated with cisplatin resistance is nucleotide excision repair (NER). There are two pathways in NER, transcription-coupled NER (TC-NER) and global genome NER (GG-NER). Here, we report that TC-NER-deficient cells [xeroderma pigmentosum group A (XP-A), XP-D, XP-F, XP-G, Cockayne syndrome group A (CS-A), and CS-B] are hypersensitive to cisplatin irrespective of their GG-NER status, and that gene complementation with XPA and XPD increases resistance to cisplatin. By contrast, XP-C cells with selective defect in GG-NER but with normal TC-NER have normal resistance to cisplatin. XPC complementation had no effect on cisplatin antiproliferative activity. We propose that one of the pathways related to cisplatin response is TC-NER, not GG-NER.




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Copyright © 2002 by the American Association for Cancer Research.