Role of glutathione in the regulation of cisplatin resistance in cancer chemotherapy

MacUs Tien Kuo, Helen H.W. Chen

研究成果: Review article同行評審

134 引文 斯高帕斯(Scopus)


Three mechanisms have been proposed for the role of glutathione (GSH) in regulating cisplatin (CDDP) sensitivities that affects its ultimate cell-killing ability: (i) GSH may serve as a cofactor in facilitating multidrug resistance protein 2- (MRP2-) mediated CDDP efflux in mammalian cells, since MRP2-transfected cells were shown to confer CDDP resistance; (ii) GSH may serve as a redox-regulating cytoprotector based on the observations that many CDDP-resistant cells overexpress GSH and -glutamylcysteine synthesis ( -GCS), the rate-limiting enzyme for GSH biosynthesis; (iii) GSH may function as a copper (Cu) chelator. Elevated GSH expression depletes the cellular bioavailable Cu pool, resulting in upregulation of the high-affinity Cu transporter (hCtr1) which is also a CDDP transporter. This has been demonstrated that overexpression of GSH by transfection with -GCS conferred sensitization to CDDP toxicity. This review describes how these three models were developed and critically reviews their importance to overall CDDP cytotoxicity in cancer cell treatments.

期刊Metal-Based Drugs
出版狀態Published - 2010

All Science Journal Classification (ASJC) codes

  • Toxicology
  • Pharmacology
  • Drug Discovery
  • Inorganic Chemistry

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