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Molecular mechanism of cell ferroptosis and research progress in regulation of ferroptosis by noncoding RNAs in tumor cells

机译:肿瘤细胞非致rNA法调节粘土性细胞裂解体和研究进展的分子机制

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摘要

Ferritin and its related genes, namely, ferritin heavy chain 1 (FTH1) and ferritin light chain (FTL), regulate the iron ion storage. Heat shock protein B1 (HSPb1) inhibits TFR1 expression to reduce the intracellular iron concentration. Therefore, ferroptosis would be inhibited by overexpression of HSPb1. Iron response element binding protein 2 (IREB2), a major transcription factor involved in iron metabolism, can significantly increase FTL and FTH1 expression, and thus inhibit erastin-induced ferroptosis. The main mechanism of biological toxicity of iron ions is mediated by the classical Fenton reaction between Fe3+ and Fe2+, which produces hydroxyl radicals that can damage DNA, lipids, and proteins, and result in ferroptosis.
机译:铁素及其相关基因,即铁蛋白重链1(Fth1)和铁蛋白轻链(FTL),调节铁离子储存。热休克蛋白B1(HSPB1)抑制TFR1表达以降低细胞内的铁浓度。因此,通过Hspb1的过表达抑制裂解子。铁响应元件结合蛋白2(IREB2),涉及铁代谢的主要转录因子,可以显着增加FTL和Fth1表达,从而抑制杂种诱导的恶性凋亡。铁离子的生物毒性的主要机制是通过Fe3 +和Fe2 +之间的经典芬顿反应介导的,这产生了可以损害DNA,脂质和蛋白质的羟基自由基,并导致铁凋亡。

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