Mitochondrial ROS in cancer: initiators, amplifiers or an Achilles' heel?
Mitochondrial ROS in cancer: initiators, amplifiers or an Achilles' heel?
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DOI：
10.1038/nrc3803
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发表时间：
2014-11
期刊：
影响因子：
--
通讯作者：
Schumacker PT
中科院分区：
文献类型：
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作者：
Sabharwal SS;Schumacker PT
线粒体通过促进生物能量学、代谢、生物合成和细胞死亡或存活功能与其宿主细胞合作。由线粒体产生的活性氧物质（ROS）参与正常细胞中的应激信号传导，但也有助于启动促进肿瘤转化的核或线粒体DNA突变。在癌细胞中，线粒体ROS放大致瘤表型，并加速导致转移行为的额外突变的积累。由于线粒体在正常细胞中发挥重要作用，因此禁用它们的功能并不是癌症的可行疗法。然而，ROS信号传导有助于许多癌症的增殖和存活，因此靶向破坏细胞与细胞的氧化还原通讯是未来治疗的一个有希望的途径。
Mitochondria cooperate with their host cells by contributing to bioenergetics, metabolism, biosynthesis, and cell death or survival functions. Reactive oxygen species (ROS) generated by mitochondria participate in stress signalling in normal cells but also contribute to the initiation of nuclear or mitochondrial DNA mutations that promote neoplastic transformation. In cancer cells, mitochondrial ROS amplify the tumorigenic phenotype and accelerate the accumulation of additional mutations that lead to metastatic behaviour. As mitochondria carry out important functions in normal cells, disabling their function is not a feasible therapy for cancer. However, ROS signalling contributes to proliferation and survival in many cancers, so the targeted disruption of mitochondria-to-cell redox communication represents a promising avenue for future therapy.