三阴性乳腺癌中凋亡铁介导的癌细胞死亡的生化机制:一种见解

Anitha Chidamabaram, Malarvili Thekkumalai, B. Prabasheela, Tripta Bhagat, J. Batra, S. Dhandayuthapani
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引用次数: 0

摘要

Ferroptosis是一种程序性细胞死亡(PCD),不同于细胞凋亡,于2012年被发现。这个过程是由依赖铁的脂质氧化变性驱动的。铁下垂通过铁依赖性脂质活性氧的积累导致细胞死亡。自由基通过氧化去除电子导致脂质分子的降解。这个过程依赖于细胞内的铁,因为铁的积累是将过氧化物转化为自由基的催化剂。当抗氧化剂谷胱甘肽的消耗和脂质修复酶谷胱甘肽过氧化物酶活性的丧失时,脂质就会发生氧化降解。脂质过氧化导致细胞膜变性。本文综述了三阴性乳腺癌独特的铁依赖性程序性细胞死亡背后的生化机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Biochemical mechanism of ferroptosis-mediated cancer cell death in triple-negative breast cancer: An insight
Ferroptosis is a form of programmed cell death (PCD), distinct from apoptosis, that was identified in 2012. The process is driven by the iron-dependent oxidative degeneration of lipids. Ferroptosis causes cell death through the accumulation of iron-dependent lipid reactive oxygen species. Free radicals cause degradation of lipid molecules by the removal of electrons through oxidation. The process is dependent on intracellular iron as the accumulation of iron acts as a catalyst for converting peroxides into free radicals. The oxidative degradation of lipids occurs when there is depletion of the antioxidant glutathione and a loss of activity of the lipid repair enzyme glutathione peroxidase 4. The lipid peroxidation then leads to cell membrane denaturation. The biochemical mechanism behind the unique iron-dependent programmed cell death with reference to the triple negative breast cancer have been reviewed in this article.
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