Transcription-coupled nucleotide excision repair as a determinant of cisplatin sensitivity of human cells

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

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271 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)4899-4902
Number of pages4
JournalCancer Research
Volume62
Issue number17
StatePublished - Sep 1 2002
Externally publishedYes

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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    Furuta, T., Ueda, T., Aune, G., Sarasin, A., Kraemer, K. H., & Pommier, Y. (2002). Transcription-coupled nucleotide excision repair as a determinant of cisplatin sensitivity of human cells. Cancer Research, 62(17), 4899-4902.