Department of Surgery, McMaster University and Juravinski Cancer Centre, Hamilton, Ontario, Canada.
Prostate Cancer Prostatic Dis. 2013 Sep;16(3):217-25. doi: 10.1038/pcan.2013.13. Epub 2013 May 14.
A mounting body of evidence suggests that increased production of reactive oxygen species (ROS) is linked to aging processes and to the etiopathogenesis of aging-related diseases, such as cancer, diabetes, atherosclerosis and degenerative diseases like Parkinson's and Alzheimer's. Excess ROS are deleterious to normal cells, while in cancer cells, they can lead to accelerated tumorigenesis. In prostate cancer (PC), oxidative stress, an innate key event characterized by supraphysiological ROS concentrations, has been identified as one of the hallmarks of the aggressive disease phenotype. Specifically, oxidative stress is associated with PC development, progression and the response to therapy. Nevertheless, a thorough understanding of the relationships between oxidative stress, redox homeostasis and the activation of proliferation and survival pathways in healthy and malignant prostate remains elusive. Moreover, the failure of chemoprevention strategies targeting oxidative stress reduced the level of interest in the field after the recent negative results of the Selenium and Vitamin E Cancer Prevention Trial (SELECT) trial. Therefore, a revisit of the concept is warranted and several key issues need to be addressed: The consequences of changes in ROS levels with respect to altered redox homeostasis and redox-regulated processes in PC need to be established. Similarly, the key molecular events that cause changes in the generation of ROS in PC and the role for therapeutic strategies aimed at ameliorating oxidative stress need to be identified. Moreover, the issues whether genetic/epigenetic susceptibility for oxidative stress-induced prostatic carcinogenesis is an individual phenomenon and what measurements adequately quantify prostatic oxidative stress are also crucial. Addressing these matters will provide a more rational basis to improve the design of redox-related clinical trials in PC. This review summarizes accepted concepts and principles in redox research, and explores their implications and limitations in PC.
越来越多的证据表明,活性氧(ROS)的产生增加与衰老过程以及与衰老相关疾病(如癌症、糖尿病、动脉粥样硬化和帕金森病和阿尔茨海默病等退行性疾病)的发病机制有关。过量的 ROS 对正常细胞有害,而在癌细胞中,它们可以导致肿瘤加速发生。在前列腺癌(PC)中,氧化应激是一种先天的关键事件,其特征是超生理 ROS 浓度,已被确定为侵袭性疾病表型的标志之一。具体而言,氧化应激与 PC 的发展、进展以及对治疗的反应有关。然而,对于健康和恶性前列腺中的氧化应激、氧化还原平衡和增殖与存活途径的激活之间的关系,人们仍未完全理解。此外,针对氧化应激的化学预防策略的失败降低了人们对该领域的兴趣,因为最近硒和维生素 E 癌症预防试验(SELECT)的阴性结果。因此,有必要重新审视这一概念,需要解决几个关键问题:需要确定 ROS 水平变化对 PC 中氧化还原平衡和氧化还原调节过程的改变的影响。同样,需要确定导致 PC 中 ROS 生成变化的关键分子事件以及旨在改善氧化应激的治疗策略的作用。此外,遗传/表观遗传易感性是否导致氧化应激诱导的前列腺癌是一个个体现象,以及哪些测量方法能充分定量前列腺氧化应激,这些问题也至关重要。解决这些问题将为改善 PC 中与氧化还原相关的临床试验设计提供更合理的基础。本文综述了氧化还原研究中公认的概念和原则,并探讨了它们在 PC 中的意义和局限性。