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丙型肝炎病毒诱发肝细胞癌的分子机制
引用本文:李冰欣,王珏,杨满意. 丙型肝炎病毒诱发肝细胞癌的分子机制[J]. 中国生物化学与分子生物学报, 2020, 36(2): 135-140. DOI: 10.13865/j.cnki.cjbmb.2019.10.1228
作者姓名:李冰欣  王珏  杨满意
作者单位:(中南大学 湘雅医院 卫生部纳米生物技术重点实验室, 长沙 410008)
基金项目:国家自然科学基金青年科学基金(No. 81402001,No. 81703412)和湖南省自然科学基金青年基金(No.2018JJ3830,No. 2016JJ3177)资助
摘    要:丙型肝炎是由丙型肝炎病毒(hepatitis C virus,HCV)引起的一种肝脏疾病。肝细胞癌(hepatocellular carcinoma,HCC)是人类最常见的恶性肿瘤之一。大量实验和临床研究表明,HCV的感染是导致肝细胞癌的主要因素之一。尽管目前可以通过直接抗病毒药物治疗HCV感染,但是患肝细胞癌的风险仍然存在。HCV诱发肝细胞癌是一个多步骤过程,其可能是通过病毒因子直接作用和/或通过引起慢性炎症诱发肝癌。因此,需要更好地了解HCV诱发肝细胞癌的分子机制,为肝细胞癌的防治提供研究基础。本文就近年来国内外对丙型肝炎病毒直接作用诱发肝细胞癌的分子机制进行综述,具体从血管生成、细胞凋亡、细胞增殖、上皮 间质转化、脂肪变性和氧化应激6个方面进行阐述,以期更好地了解HCV诱发肝细胞癌的分子机制,为肝细胞癌的防治提供研究基础。

关 键 词:丙型肝炎病毒     肝细胞癌   分子机制  
收稿时间:2019-05-28

Molecular Mechanisms of Hepatocellular Carcinoma Induced by the Hepatitis C Virus
LI Bing-Xin,WANG Jue,YANG Man-Yi. Molecular Mechanisms of Hepatocellular Carcinoma Induced by the Hepatitis C Virus[J]. Chinese Journal of Biochemistry and Molecular Biology, 2020, 36(2): 135-140. DOI: 10.13865/j.cnki.cjbmb.2019.10.1228
Authors:LI Bing-Xin  WANG Jue  YANG Man-Yi
Affiliation:(Key Laboratory of Nanobiological Technology of Chinese Ministry of Health, Xiangya Hospital, ;Central South University, Changsha 410008, China)
Abstract:Hepatitis C is a liver disease caused by the hepatitis C virus (HCV). Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in humans. A large number of experimental and clinical studies have shown that HCV infection is one of the main factors leading to HCC. HCV-induced HCC is a multi-step process that may be directly induced by viral factors and/or induced by chronic inflammation. Although HCV infection can currently be treated by direct antiviral drugs, the risk of HCC remains. Therefore, it is necessary to better understand the molecular mechanism of HCV-induced HCC to provide a research basis for the prevention and treatment of HCC. In this study, we summarize the molecular mechanisms of HCC induced by direct action of HCV from six aspects: angiogenesis, apoptosis, cell proliferation, epithelial-mesenchymal transition, steatosis and oxidative stress.
Keywords:hepatitis C virus(HCV)   hepatocellular carcinoma(HCC)   molecular mechanisms  
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