Hepatitis B virus X protein induces malignant transformation of hepatic oval cells

廖凯; 王月飞; 卢乐乐; 张雷达

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Hepatitis B virus X protein induces malignant transformation of hepatic oval cells

更新时间：2026-01-09

- Hepatitis B virus X protein induces malignant transformation of hepatic oval cells
- Journal of Army Medical University Vol. 36, Issue 10, Pages: 992-995(2014)
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  CLC： R322.47;R373.21;R394.3
- Published：2014
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廖凯,王月飞,卢乐乐,张雷达.乙型肝炎病毒X蛋白诱导肝卵圆细胞恶性转化[J].陆军军医大学学报(原第三军医大学学报),2014,36(10):992-995.

　Liao Kai,Wang Yuefei,Lu Lele,Zhang Leida.Hepatitis B virus X protein induces malignant transformation of hepatic oval cells[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(10):992-995.
廖凯,王月飞,卢乐乐,张雷达.乙型肝炎病毒X蛋白诱导肝卵圆细胞恶性转化[J].陆军军医大学学报(原第三军医大学学报),2014,36(10):992-995. DOI：

　Liao Kai,Wang Yuefei,Lu Lele,Zhang Leida.Hepatitis B virus X protein induces malignant transformation of hepatic oval cells[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(10):992-995. DOI：

摘要

目的研究乙型肝炎病毒X蛋白（hepatitis B virus X

HBx）对肝卵圆细胞的转化作用。方法构建表达HBx和嘌呤霉素抗性的慢病毒LV-HBx-PM及对照慢病毒LV-PM分别感染WB-F344肝卵圆细胞。以感染HBx慢病毒载体的WB-F344细胞作为实验组（WB-F344-HBx），以感染对照慢病毒载体的WB-F344细胞作为阴性对照组（WB-F344-PM），以未转染慢病毒载体的培养相同代数的WB-F344细胞作为空白对照组（WB-F344-Mock）。通过Real-time RT-PCR和Western blot验证各组细胞中HBx的表达；运用MTT法、流式细胞术、细胞迁移实验、裸鼠移植瘤实验观察各组细胞的增殖能力、细胞周期、迁移能力和成瘤能力。结果 WB-F344-HBx细胞在基因水平和蛋白水平稳定高效表达HBx；WB-F344-PM和WB-F344-Mock不表达HBx。与阴性对照组WB-F344-PM相比，实验组WB-F344-HBx G

期细胞比例降低[（55.98±0.39）% vs (61.65±1.37)%

0.01

]

，G

/M期细胞比例升高[（15.05±1.67)% vs (7.83±0.46)%，

0.01

]

，细胞周期进程加快，细胞增殖能力增强（

0.01），具有更强的细胞迁移能力和成瘤能力；而阴性对照组WB-F344-PM与空白对照组WB-F344-Mock相比，细胞周期、细胞增殖能力、细胞迁移能力和成瘤能力无显著变化。 结论乙型肝炎病毒X蛋白可诱导肝卵圆细胞恶性转化。

Abstract

Objective Detect the malignant transformation of hepatic oval cells induced by hepatitis B virus X (HBx) protein. Methods Hepatic oval cells

WB-F344 cells

transfected with lentivirus expressing HBx and puromycin (PM)-resistant gene were defined as an experimental group (WB-F344-HBx). The WB-F344 cells transfected with lentivirus o

nly expressing PM-resistant gene were defined as a negative control group (WB-F344-PM). The WB-F344 cells without lentivirus transfection were defined as a blank control group (WB-F344-Mock). The expressions of HBx in the 3 groups were confirmed by real-time RT-PCR and Western blotting. The cell cycle

proliferation

ability of metastasis and tumorigenicity were detected with flow cytometry

MTT assay

metastasis experiment and nude mouse transplantation tumor experiment

respectively. Results Highly stably HBx protein expression was observed in the experimental group but not in the negative control and blank control groups. Compared with the negative control group

the experimental group showed decreased G

cell percentage [(55.98±0.39)% vs （61.65±1.37）%

0.01)

increased G

/M cell percentage [(15.05±1.67)% vs （7.83±0.46）%

0.01

]

significantly accelerated process of G

/S cell cycle

promoted cell proliferation (

0.01)

and increased ability of metastasis and tumorigenicity. There was no significant difference in cell cycle

cell proliferation

ability of metastasis and tumorigenicity between the negative control group and the blank control group. Conclusion Hepatitis B virus X protein can induce malignant transformation of hepatic oval cells.

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