Sazonova Elena V, Kopeina Gelina S, Imyanitov Evgeny N, Zhivotovsky Boris
Faculty of Medicine, MV Lomonosov Moscow State University, Moscow, 119991, Russia.
Department of Tumor Growth Biology, N.N. Petrov Institute of Oncology, St.-Petersburg, 197758, Russia.
Cell Death Discov. 2021 Jun 26;7(1):155. doi: 10.1038/s41420-021-00554-5.
Cancer therapy is aimed at the elimination of tumor cells and acts via the cessation of cell proliferation and induction of cell death. Many research publications discussing the mechanisms of anticancer drugs use the terms "cell death" and "apoptosis" interchangeably, given that apoptotic pathways are the most common components of the action of targeted and cytotoxic compounds. However, there is sound evidence suggesting that other mechanisms of drug-induced cell death, such as necroptosis, ferroptosis, autophagy, etc. may significantly contribute to the fate of cancer cells. Molecular cross-talks between apoptotic and nonapoptotic death pathways underlie the successes and the failures of therapeutic interventions. Here we discuss the nuances of the antitumor action of two groups of the widely used anticancer drugs, i.e., platinum salts and taxane derivatives. The available data suggest that intelligent interference with the choice of cell death pathways may open novel opportunities for cancer treatment.
癌症治疗旨在消除肿瘤细胞，其作用途径是停止细胞增殖并诱导细胞死亡。鉴于凋亡途径是靶向化合物和细胞毒性化合物作用中最常见的组成部分，许多讨论抗癌药物作用机制的研究出版物都将“细胞死亡”和“凋亡”这两个术语互换使用。然而，有充分的证据表明，药物诱导细胞死亡的其他机制，如坏死性凋亡、铁死亡、自噬等，可能对癌细胞的命运有显著影响。凋亡和非凋亡死亡途径之间的分子相互作用是治疗干预成败的基础。在这里，我们讨论两组广泛使用的抗癌药物，即铂盐和紫杉烷衍生物的抗肿瘤作用细微差别。现有数据表明，对细胞死亡途径选择进行明智干预可能为癌症治疗带来新的机遇。
