Restoration of mitochondria function as a target for cancer therapy.
Restoration of mitochondria function as a target for cancer therapy.
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DOI：
10.1016/j.drudis.2015.03.001
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发表时间：
2015-05
影响因子：
7.4
通讯作者：
Chandra D
中科院分区：
文献类型：
--
作者：
Bhat TA;Kumar S;Chaudhary AK;Yadav N;Chandra D
氧化磷酸化缺陷在线粒体功能减弱中起着至关重要的作用，这赋予癌症的治疗抗性。各种因素，包括内源性热休克蛋白（HSP）和外源性试剂，如二氯乙酸，恢复呼吸和其他生理功能的线粒体在癌细胞。功能性线粒体可能最终导致对当前抗癌剂难治的癌细胞凋亡的恢复。在这里，我们总结了导致癌细胞中线粒体功能障碍的关键原因，以及线粒体功能的恢复是否和/或如何用于癌症治疗。
Defective oxidative phosphorylation has a crucial role in the attenuation of mitochondrial function, which confers therapy resistance in cancer. Various factors, including endogenous heat shock proteins (HSPs) and exogenous agents such as dichloroacetate, restore respiratory and other physiological functions of mitochondria in cancer cells. Functional mitochondria might ultimately lead to the restoration of apoptosis in cancer cells that are refractory to current anticancer agents. Here, we summarize the key reasons contributing to mitochondria dysfunction in cancer cells and whether and/or how restoration of mitochondrial function could be exploited for cancer therapeutics.