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活性氧物种在结直肠癌发生发展中的作用:诊疗方法的视角

The Role of Reactive Oxygen Species in Colorectal Cancer Initiation and Progression: Perspectives on Theranostic Approaches.

作者信息

Catalano Teresa, Selvaggi Federico, Cotellese Roberto, Aceto Gitana Maria

机构信息

Department of Clinical and Experimental Medicine, University of Messina, Via Consolare Valeria, 98125 Messina, Italy.

Villa Serena Foundation for Research, 65013 Città Sant'Angelo, Italy.

出版信息

Cancers (Basel). 2025 Feb 22;17(5):752. doi: 10.3390/cancers17050752.

DOI:10.3390/cancers17050752
PMID:40075600
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11899472/
Abstract

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.

摘要

活性氧(ROS)水平的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、发展和复发/转移中发挥作用。肿瘤细胞可通过长期或短期的基因或代谢重编程来适应氧化应激(OS)。此外,肿瘤细胞通过对抗氧化分子的正向调节来保护自身,增强ROS驱动的增殖。平衡的氧化应激水平可影响化疗耐药性,使肿瘤细胞在治疗中存活。化疗的副作用包括ROS产生增加和氧化还原应激,这可杀死癌细胞并消除耐药性。基于调控ROS水平的抗癌治疗可能代表CRC治疗的金标准。因此,探索在失调信号通路中对OS反应的调节可能会导致开发新的个性化CRC治疗方法以克服治疗耐药性。在本综述中,我们探讨了ROS在CRC发生和发展中的作用及其作为疾病生物标志物的诊断意义。此外,我们重点关注了ROS在不同CRC治疗选择中的作用,如手术、放疗、诊疗成像、化疗和免疫治疗以及其他精准医学方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bbd/11899472/f0791453d26c/cancers-17-00752-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bbd/11899472/e915a4ca9e4d/cancers-17-00752-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bbd/11899472/f0791453d26c/cancers-17-00752-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bbd/11899472/e915a4ca9e4d/cancers-17-00752-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bbd/11899472/f0791453d26c/cancers-17-00752-g002.jpg

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