Oxidative Stress, Redox Signaling, and Apoptosis in Prostate Cancer Development and Progression

Prostate cancer (PC) is one of the most common tumors in the male population. One of the possible causes of cancer is reactive oxygen species (ROS). They can be involved in all stages of tumor growth. There are a lot of different inducers of ROS. Xanthine oxidase (XO) is the enzyme that can be responsible for oxidative damage in cancer, since free radicals are also a side product of this enzyme’s activity. The results of some studies showed more than twice the activity of XO when compared to control tissue and tissue surrounding the tumor compared to control healthy tissue. It is even strongly correlated with the PSA values from the patients’ serum. This suggests XO as a potential marker in the diagnosis of the disease. The inhibition of this enzyme has been investigated as a possible direct target therapy for cancer, so it could be a theranostic marker. ROS can also participate in carcinogenesis through redox-dependent signaling pathways. The transcription factor NF-kB is a regulatory protein that controls the expression of many inducible and tissue-specific genes, thereby participating in the regulation of pro-inflammatory and immune cell responses, cell proliferation, and apoptosis. NF-κB signaling may also be crucial in tumor progression. The inhibition of signaling pathways originating from the activity of this redox-sensitive molecule could be a promising therapeutic strategy, by inhibiting the IKK subunit of NF-κB. Both ROS and NF-κB can be inducers and blockers of apoptosis. Apoptosis has an important function in the removal of damaged cells. Failure of apoptosis may be an important factor in the evolution of PC and poor response to chemotherapy and radiation therapy. The novel apoptosis inhibitors have been introduced, and they appear to have a role in prostate cancer treatment resistance. Therapeutic effect on apoptosis could be one of the possible therapies for this disease.