Laboratory for Genotoxic Agents, Division of Molecular Biology, Rudjer Boskovic Institute, Zagreb, Croatia.
Crit Rev Toxicol. 2010 Apr;40(4):347-59. doi: 10.3109/10408441003601836.
Cisplatin (cDDP) is an anticancer agent that is widely used in the treatment of many solid tumors. A major obstacle to successful cDDP-based chemotherapy, however, is the intrinsic and acquired resistance of tumor cells to this drug. Greater insight into the molecular mechanisms underlying the modulation of cellular responses to cDDP will aid in the development and optimization of new therapeutic strategies. Apart from induction of DNA damage, recent data have suggested that cDDP also induces the formation of reactive oxygen species that can trigger cell death. Cell death occurs as the result of several simultaneously activated signaling pathways. The specific pathway responsible for cell death depends on the cell type and the treatment conditions. This review focuses on the relationship between glutathione and BCL-2 and their protective role in cDDP-induced reactive oxygen species formation and cDDP resistance.
顺铂（cDDP）是一种广泛用于治疗多种实体瘤的抗癌药物。然而，肿瘤细胞对这种药物的内在和获得性耐药是成功进行基于顺铂的化疗的主要障碍。深入了解调节细胞对顺铂反应的分子机制将有助于开发和优化新的治疗策略。除了诱导 DNA 损伤外，最近的数据还表明，顺铂还诱导活性氧的形成，从而触发细胞死亡。细胞死亡是几种同时激活的信号通路的结果。负责细胞死亡的特定途径取决于细胞类型和治疗条件。这篇综述重点介绍了谷胱甘肽和 BCL-2 之间的关系及其在顺铂诱导的活性氧形成和顺铂耐药中的保护作用。
