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Int J Mol Sci. 2011;12(10):7163-85. doi: 10.3390/ijms12107163. Epub 2011 Oct 21.

Mitochondrial peroxiredoxin III is a potential target for cancer therapy.

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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: (I.-S.S.); (H.-K.K.); (S.-H.J.); (S.-R.L.); (N.K.); (B.D.R.); (K.S.K.).


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.


ROS; antioxidant; cancer; mitochondria; oxidative stress; peroxiredoxin III; therapy

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