氧化应激与非小细胞肺癌关系的研究进展

Research progress in the relationship between oxidative stress and NSCLC

非小细胞肺癌(NSCLC)患者逐年增加,且手术等传统治疗方法效果有限。肺作为呼吸系统的核心器官,负责机体与外界的气体交换,外界导入的活性氧与内源性的抗氧化体系失衡共同导致肺部容易出现氧化应激损伤。氧化应激所产生的低浓度活性氧(ROS)参与了肺部肿瘤特别是NSCLC的发生与发展,而高浓度的ROS又可启动肿瘤细胞的自噬凋亡进程,并能促进NSCLC细胞对放化疗的敏感性。从氧化应激所产生的低浓度ROS所造成的线粒体损伤、促进肿瘤血管形成和细胞信号通路异常出发,系统梳理了氧化应激在肺癌发生和发展中的作用,讨论肿瘤细胞如何通过抗氧化通路的激活对ROS进行利用,同时探讨高浓度ROS在NSCLC治疗中所展现出的积极作用。

The number of non-small cell lung cancer(NSCLC)patients increase year by year,and traditional treatment methods such as surgery have limited effect.Lungs as the core organ of the respiratory system,are responsible for the exchange of air between the body and the outside world.The active oxygen introduced from the outside and the imbalance of the endogenous antioxidant system together cause the lung to be prone to oxidative stress damage.The low concentration of reactive oxygen species(ROS)produced by oxidative stress is involved in the occurrence and development of lung tumors,especially NSCLC.The high concentration of ROS can initiate the autophagic apoptosis of tumor cells and promote the sensitivity of NSCLC cells to radiotherapy and chemotherapy.In this review paper,the mitochondrial damage,the promoting tumor angiogenesis and abnormal cell signaling pathways caused by low concentration of ROS generated by oxidative stress were summarized.The role of oxidative stress in the occurrence and development of lung cancer was systematically sorted out.The mechanism of tumor cells using ROS to activate antioxidant pathways was discussed,and the positive effects of high-concentration ROS in NSCLC treatment were discussed.