氧化应激在肝细胞癌发展中的作用

Yuanyuan Li, Yang Yu, Lei Yang, Rui Wang
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引用次数: 0

摘要

氧化应激(OS)与肝细胞癌(HCC)的进展有关。HCC可能是遗传改变的结果,包括核和线粒体DNA的氧化损伤。由OS调节的信号通路,如Wnt/β-catenin和Notch通路,是HCC发生的重要调节因子。os介导的转录因子的激活,包括核因子-κB和p53等,能够调节HCC细胞的氧化还原状态。OS还影响肿瘤微环境,进而调节HCC的进展。在HCC中,活性氧(ROS)可以潜在地增强肿瘤细胞的增殖、转移和对治疗的抵抗。然而,在HCC细胞中,ROS水平升高可引起细胞毒性并引发细胞凋亡。这篇综述强调并探讨了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。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Insights into the Role of Oxidative Stress in Hepatocellular Carcinoma Development
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.
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