Altered levels of reactive oxygen species (ROS) are recognized as one of the key factors in mediating tumor cell survival in the tissue microenvironment, where they play a role in the initiation, progression and recurrence/relapse of colorectal cancer (CRC). Tumor cells can adapt to oxidative stress (OS) using genetic or metabolic reprogramming in the long or short term. In addition, tumor cells defend themselves through positive regulation of antioxidant molecules, enhancing ROS-driven proliferation. Balanced oxidative eustress levels can influence chemotherapy resistance, allowing tumor cells to survive treatment. Secondary effects of chemotherapy include increased ROS production and redox stress, which can kill cancer cells and eliminate drug resistance. Anticancer treatments based on manipulating ROS levels could represent the gold standard in CRC therapy. Therefore, exploring the modulation of the response to OS in deregulated signaling pathways may lead to the development of new personalized CRC treatments to overcome therapy resistance. In this review, we explore the role of ROS in the initiation and progression of CRC and their diagnostic implications as biomarkers of disease. Furthermore, we focused on the involvement of ROS in different CRC therapeutic options, such as surgery, radiotherapy, theranostic imaging, chemotherapy and immunotherapy and other precision medicine approaches.
活性氧（ROS）水平改变被认为是介导肿瘤细胞在组织微环境中存活的关键因素之一，在结直肠癌（CRC）的发生、进展及复发/转移过程中发挥重要作用。肿瘤细胞可通过长期或短期的遗传或代谢重编程适应氧化应激（OS）。此外，肿瘤细胞通过正向调控抗氧化分子进行自我防御，从而增强ROS驱动的增殖效应。平衡的氧化良性应激水平可影响化疗耐药性，使肿瘤细胞在治疗中得以存活。化疗的继发效应包括ROS生成增加和氧化还原应激增强，这些反应既能杀伤癌细胞，也能消除耐药性。基于调控ROS水平的抗癌治疗可能成为CRC治疗的金标准。因此，探索失调信号通路中氧化应激反应的调控机制，有望开发出新型个体化CRC治疗方案以克服治疗耐药性。本综述探讨了ROS在CRC发生发展中的作用及其作为疾病生物标志物的诊断价值，并重点阐述了ROS在不同CRC治疗方案中的参与机制，包括手术治疗、放射治疗、诊疗一体化成像、化学治疗、免疫治疗及其他精准医学方法。
肿瘤(癌症)患者之家