National Research Laboratory for Mitochondrial Signaling, Department of Physiology, College of Medicine, Cardiovascular and Metabolic Disease Center, Inje University, Busan 614-7-5, Korea; E-Mails:
Int J Mol Sci. 2011;12(10):7163-85. doi: 10.3390/ijms12107163. Epub 2011 Oct 21.
Mitochondria are involved either directly or indirectly in oncogenesis and the alteration of metabolism in cancer cells. Cancer cells contain large numbers of abnormal mitochondria and produce large amounts of reactive oxygen species (ROS). Oxidative stress is caused by an imbalance between the production of ROS and the antioxidant capacity of the cell. Several cancer therapies, such as chemotherapeutic drugs and radiation, disrupt mitochondrial homeostasis and release cytochrome c, leading to apoptosome formation, which activates the intrinsic pathway. This is modulated by the extent of mitochondrial oxidative stress. The peroxiredoxin (Prx) system is a cellular defense system against oxidative stress, and mitochondria in cancer cells are known to contain high levels of Prx III. Here, we review accumulating evidence suggesting that mitochondrial oxidative stress is involved in cancer, and discuss the role of the mitochondrial Prx III antioxidant system as a potential target for cancer therapy. We hope that this review will provide the basis for new strategic approaches in the development of effective cancer treatments.
线粒体直接或间接地参与了肿瘤的发生和癌细胞代谢的改变。癌细胞含有大量异常的线粒体,并产生大量的活性氧(ROS)。氧化应激是由 ROS 的产生与细胞抗氧化能力之间的失衡引起的。几种癌症疗法,如化疗药物和辐射,破坏了线粒体的内稳态并释放细胞色素 c,导致凋亡小体的形成,从而激活内在途径。这一过程受到线粒体氧化应激程度的调节。过氧化物酶(Prx)系统是细胞抵抗氧化应激的防御系统,已知癌细胞中的线粒体含有高水平的 Prx III。在这里,我们回顾了越来越多的证据表明,线粒体氧化应激与癌症有关,并讨论了线粒体 Prx III 抗氧化系统作为癌症治疗潜在靶点的作用。我们希望这篇综述将为开发有效癌症治疗方法的新战略方法提供基础。