Oxidative stress as a catalyst in prostate cancer progression: unraveling molecular mechanisms and exploring therapeutic interventions.

Prostate cancer is the second most common malignancy among men worldwide, with its incidence and mortality rates steadily increasing. Although androgen deprivation therapy (ADT) combined with androgen receptor inhibitors has shown significant efficacy in treating prostate cancer, resistance to treatment remains a major challenge, particularly in patients with metastatic prostate cancer. Reactive oxygen species (ROS), a class of highly reactive molecules, can induce oxidative stress within cells, thereby affecting cellular survival and function. In cancer cells, elevated ROS levels not only promote proliferation and invasion but also contribute to the malignancy of tumors by modulating the tumor microenvironment, enhancing angiogenesis, and facilitating extracellular matrix remodeling. This review systematically explores the pathways of ROS generation in prostate cancer, their interaction with the androgen receptor signaling pathway, and the role of external factors such as obesity and aging in promoting ROS production. The findings highlight that ROS drive prostate cancer progression through multiple mechanisms, including altering the tumor microenvironment, activating the unfolded protein response (UPR), and regulating miRNA expression. By providing a comprehensive analysis of ROS-mediated mechanisms in prostate cancer, this review offers new insights into the development of targeted antioxidant therapeutic strategies.