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首页> 外文期刊>International Journal of Surgical Oncology >Mechanisms of Cisplatin-Induced Apoptosis and of Cisplatin Sensitivity: Potential of BIN1 to Act as a Potent Predictor of Cisplatin Sensitivity in Gastric Cancer Treatment
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Mechanisms of Cisplatin-Induced Apoptosis and of Cisplatin Sensitivity: Potential of BIN1 to Act as a Potent Predictor of Cisplatin Sensitivity in Gastric Cancer Treatment

机译：顺铂诱导的细胞凋亡和顺铂敏感性的机制：BIN1可能作为胃癌治疗中顺铂敏感性的潜在预测因子。

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Cisplatin is the most important and efficacious chemotherapeutic agent for the treatment of advanced gastric cancer. Cisplatin forms inter- and intrastrand crosslinked DNA adducts and its cytotoxicity is mediated by propagation of DNA damage recognition signals to downstream pathways involving ATR, p53, p73, and mitogen-activated protein kinases, ultimately resulting in apoptosis. Cisplatin resistance arises through a multifactorial mechanism involving reduced drug uptake, increased drug inactivation, increased DNA damage repair, and inhibition of transmission of DNA damage recognition signals to the apoptotic pathway. In addition, a new mechanism has recently been revealed, in which the oncoprotein c-Myc suppresses bridging integrator 1 (BIN1), thereby releasing poly(ADP-ribose)polymerase 1, which results in increased DNA repair activity and allows cancer cells to acquire cisplatin resistance. The present paper focuses on the molecular mechanisms of cisplatin-induced apoptosis and of cisplatin resistance, in particular on the involvement of BIN1 in the maintenance of cisplatin sensitivity.
机译：顺铂是治疗晚期胃癌最重要，最有效的化学治疗剂。顺铂形成链内和链内交联的DNA加合物，其细胞毒性由DNA损伤识别信号传播到涉及ATR，p53，p73和促分裂原活化蛋白激酶的下游途径而介导，最终导致细胞凋亡。顺铂耐药性是由多因素机制引起的，包括减少药物吸收，增加药物失活，增加DNA损伤修复以及抑制DNA损伤识别信号向凋亡途径的传递。此外，最近发现了一种新的机制，其中癌蛋白c-Myc抑制桥整合子1（BIN1），从而释放出聚（ADP-核糖）聚合酶1，这导致DNA修复活性增强，并使癌细胞获得顺铂耐药性。本文着眼于顺铂诱导的细胞凋亡和顺铂耐药的分子机制，特别是BIN1参与维持顺铂敏感性。

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