REVIEW: Oxidative Stress and Redox-Dependent Signaling in Prostate Cancer

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Elena V. Kalinina^1,a*, Ludmila A. Gavriliuk¹, and Vadim S. Pokrovsky^1,2

¹Peoples’s Friendship University of Russia (RUDN University), 117198 Moscow, Russia

²N. N. Blokhin National Medical Research Center of Oncology, 115478 Moscow, Russia

^* To whom correspondence should be addressed.

Received January 24, 2022; Revised March 20, 2022; Accepted March 20, 2022

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Tumor emergence and progression is complicated by the dual role of reactive oxygen species (ROS). Low concentrations of ROS are essential for many intracellular metabolic processes and cell proliferation, while excessive ROS generation disrupts the mechanisms of cancer suppression, leading to the cell damage and death. A long-term imbalance in the ROS/antioxidant ratio and upregulation of the ROS generation due to the reduced efficacy of the antioxidant defense system cause chronic oxidative stress resulting in the damage of proteins, lipid, and DNA molecules and cancer development. Numerous data demonstrate that prostate cancer (the most common cancer in males) is associated with the development of oxidative stress. However, the reasons for the emergence of prostate cancer, as well as changes in the redox signaling and cellular redox homeostasis in this disease, are still poorly understood. The review examines the role of prooxidant and antioxidant enzyme systems, the imbalance in their activity leading to the oxidative stress development, changes in the key components of redox signaling, and the role of microRNAs in the modulation of redox status of cancer cells in prostate cancer.

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KEY WORDS: prostate cancer, oxidative stress, antioxidant and prooxidant enzymes, transcription factors, Nrf2, NF-κB, redox-dependent signaling, microRNA

DOI: 10.1134/S0006297922050030

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