Li Yuanyuan, Yu Yang, Yang Lei, Wang Rui
Department of Medical Oncology, Affiliated Tumor Hospital, Nantong University, 226300 Nantong, Jiangsu, China.
Department of Medical Oncology, Affiliated Jinling Hospital, Medical School of Nanjing University, 210016 Nanjing, Jiangsu, China.
Front Biosci (Landmark Ed). 2023 Nov 8;28(11):286. doi: 10.31083/j.fbl2811286.
Oxidative stress (OS) is linked to hepatocellular carcinoma (HCC) progression. HCC may develop as a result of genetic changes, including oxidative injury to both nuclear and mitochondrial DNA. Signaling pathways regulated by OS, such as Wnt/β-catenin and Notch pathways, are vital regulators in developing HCC. OS-mediated activation of transcription factors, including nuclear factor-κB and p53, among others, is capable of regulating the redox state of HCC cells. OS also affects the tumor microenvironment, which, in turn, regulates HCC progression. In HCC, reactive oxygen species (ROS) can potentially enhance tumor cell proliferation, metastasis, and resistance to treatment. However, elevated ROS levels can cause cytotoxicity and trigger apoptosis in HCC cells. This review highlights and explores potential oxidative stress-related treatment targets in HCC, offering novel insights for clinical therapies.
氧化应激（OS）与肝细胞癌（HCC）的进展相关。HCC可能是由基因变化引起的，包括对核DNA和线粒体DNA的氧化损伤。由OS调节的信号通路，如Wnt/β-连环蛋白和Notch通路，是HCC发生发展中的重要调节因子。OS介导的转录因子激活，包括核因子-κB和p53等，能够调节HCC细胞的氧化还原状态。OS还会影响肿瘤微环境，而肿瘤微环境又会反过来调节HCC的进展。在HCC中，活性氧（ROS）可能会增强肿瘤细胞的增殖、转移和对治疗的抗性。然而，ROS水平升高会导致细胞毒性并触发HCC细胞凋亡。本综述重点介绍并探讨了HCC中潜在的氧化应激相关治疗靶点，为临床治疗提供了新的见解。
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