线粒体
细胞凋亡
程序性细胞死亡
心磷脂
细胞生物学
生物
癌细胞
自噬
细胞
线粒体通透性转换孔
粒体自噬
癌症研究
癌症
生物化学
遗传学
膜
磷脂
作者
Gustavo Ferrín,Clara I. Linares,Jordi Muntané
标识
DOI:10.2174/138161211796904803
摘要
Mitochondria are involved in different physiological and pathological processes that are crucial for tumor cell physiology, growth and survival. Since cancer cells have frequently disrupted different cell death pathways that promote their survival, mitochondria may be key organelles to promote cell death in cancer cells. The present review is focused on the different experimental and therapeutic cancer strategies addressed to either target mitochondria directly, or use mitochondria as mediators of apoptosis. While the first group includes drugs that act on glycolysis, β-oxidation, electron transport chain, mitochondrial permeability and the Bcl-2/IAP family protein, the second one consists of those drugs that cause cell death through the intrinsic apoptosis pathway by promoting ROS generation or by modulating mitochondrial protein involved in apoptosis induction. Keywords: Apoptosis, metabolism, oxidative stress, therapy, anti-tumoral therapy, cardiolipin, DNA fragmentation, Vitamin E, caspases, glycolysis
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