Activation of programmed cell death by anticancer agents: cisplatin as a model system.

IF 3.5 Q1 DENTISTRY, ORAL SURGERY & MEDICINE
A Eastman
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Abstract

The anticancer drug cisplatin exerts its action as a consequence of interaction with DNA. Cell cycle progression facilitates sensitivity to the drug, but inhibition of DNA synthesis is not necessarily the critical step. Lethally damaged cells can progress to and arrest for several days in the G2 phase of the cell cycle before dying. Certain features of cisplatin-induced cell death, such as chromatin condensation and the activation of a DNA endonuclease, are reminiscent of apoptosis, or programmed cell death. Many other anticancer drugs produce the same phenotypic effects, suggesting that these agents may all interact with the same signal transduction pathway leading to cell death.

抗癌药物激活程序性细胞死亡:以顺铂为模型系统。
抗癌药物顺铂是与DNA相互作用的结果。细胞周期的进展促进了对药物的敏感性,但抑制DNA合成并不一定是关键步骤。在死亡之前,致命损伤的细胞可以进展到细胞周期的G2期,并在G2期停留数天。顺铂诱导的细胞死亡的某些特征,如染色质凝结和DNA内切酶的激活,使人想起细胞凋亡或程序性细胞死亡。许多其他抗癌药物产生相同的表型效应,表明这些药物可能都与导致细胞死亡的相同信号转导途径相互作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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