Song Yawen, Hou Zheng, Zhu Longting, Chen Yan, Li Jingyu
Department of Urology, Xijing Hospital of Air Force Military Medical University, Xi'an, China.
Department of Urology, Dandong Central Hospital, 70 Renmin Road, Zhenxing District, Dandong, 118000, Liaoning, China.
Discov Oncol. 2025 Apr 3;16(1):457. doi: 10.1007/s12672-025-02245-4.
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.
前列腺癌是全球男性中第二常见的恶性肿瘤，其发病率和死亡率呈稳步上升趋势。尽管雄激素剥夺疗法（ADT）联合雄激素受体抑制剂在治疗前列腺癌方面已显示出显著疗效，但治疗耐药性仍然是一个主要挑战，尤其是在转移性前列腺癌患者中。活性氧（ROS）是一类高反应性分子，可诱导细胞内的氧化应激，从而影响细胞存活和功能。在癌细胞中，升高的ROS水平不仅促进增殖和侵袭，还通过调节肿瘤微环境、增强血管生成和促进细胞外基质重塑来促进肿瘤的恶性发展。本综述系统地探讨了前列腺癌中ROS产生的途径、它们与雄激素受体信号通路的相互作用，以及肥胖和衰老等外部因素在促进ROS产生中的作用。研究结果强调，ROS通过多种机制驱动前列腺癌进展，包括改变肿瘤微环境、激活未折叠蛋白反应（UPR）和调节miRNA表达。通过对前列腺癌中ROS介导机制的全面分析，本综述为靶向抗氧化治疗策略的开发提供了新的见解。
