Objective: To explore the internal mechanism of hepatocellular carcinoma (HCC) induced by chronic hepatitis B virus (HBV) infection.
Methods: L02, HepG2 and Huh7 cells stably overexpressing HBV preS1 antigen were analyzed by flow cytometry, qRT-PCR and tumorigenesis in nude mice to evaluate the effect of preS1 antigen in HBV-related hepatocarcinogenesis.
Results: Our results showed that the expression of cancer stem cell (CSCs) related factors and cell surface markers in preS1 overexpressing cells were up-regulated, and the tumorigenicity of these cells was enhanced in nude mice. In addition, preS1 overexpression could down-regulate the expression of major histocompatibility complex Ⅰ (MHC-Ⅰ). The expression of MHC-Ⅰ on the cell surface could be restored by adding interferon gamma (IFN-γ) in the process of cell culturing and the tumorigenicity of cells in nude mice could thus be reduced.
Conclusion: Based on the above results, we believe that preS1 is a carcinogen of HBV and that it promotes the formation of liver cancer through down regulating MHC-Ⅰ on the surface of hepatocytes.
目的: 探讨慢性乙型肝炎病毒（HBV）感染诱发肝癌所涉及的内在机制。
方法: 对稳定过表达HBV前S1抗原（preS1）的L02、HepG2和Huh7细胞进行流式细胞术、实时荧光定量和裸鼠成瘤等实验来评估preS1在HBV相关性肝癌发生中的作用。
结果: preS1诱导细胞肿瘤干细胞（CSCs）相关因子和表面标志分子的表达上调，增强细胞的裸鼠成瘤能力；过表达preS1可以下调细胞表面组织相容性复合体Ⅰ（MHC-Ⅰ）的表达；在细胞培养过程中加入γ干扰素（IFN-γ）可以恢复细胞表面MHC-Ⅰ的表达，降低细胞的裸鼠成瘤能力。
结论: preS1是HBV的一个致癌因子，通过下调肝细胞表面MHC I促进肝癌产生。
Keywords: Hepatitis B virus; Hepatocellular carcinoma; Histocompatibility complex Ⅰ (MHC-Ⅰ); Interferon gamma (IFN-γ); preS1 antigen of HBV.
Copyright© by Editorial Board of Journal of Sichuan University (Medical Sciences).