Mitochondrial Peroxiredoxin III is a Potential Target for Cancer Therapy

International Journal of Molecular Sciences

In-Sung Song¹  Hyoung-Kyu Kim¹  Seung-Hun Jeong¹  Sung-Ryul Lee¹  Nari Kim¹  Byoung Doo Rhee¹  Kyung Soo Ko¹ 

[1] National Research Laboratory for Mitochondrial Signaling, Department of Physiology, College of Medicine, Cardiovascular and Metabolic Disease Center, Inje University, Busan 614-7-5, Korea;

关键词: ROS;    mitochondria;    peroxiredoxin III;    cancer;    antioxidant;    oxidative stress;    therapy;   

DOI  :  10.3390/ijms12107163

来源: mdpi

【 摘 要 】

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.

【 授权许可】

CC BY   
© 2011 by the authors; licensee MDPI, Basel, Switzerland.