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)

摘要

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.

原文English
文章編號430939
期刊Metal-Based Drugs
2010
DOIs
出版狀態Published - 2010

All Science Journal Classification (ASJC) codes

  • Toxicology
  • Pharmacology
  • Drug Discovery
  • Inorganic Chemistry

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