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Start Over Author "Shen, Zhongliang" Topic hbx
3 results on '"Shen, Zhongliang"'

2. Identification of Estradiol Benzoate as an Inhibitor of HBx Using Inducible Stably Transfected HepG2 Cells Expressing HiBiT Tagged HBx.

Author

He, Jingjing, Wu, Jingwen, Chen, Jingwen, Zhang, Shenyan, Guo, Yifei, Zhang, Xueyun, Han, Jiajia, Zhang, Yao, Guo, Yue, Lin, Yanxue, Yu, Weien, Kong, Yide, Shen, Zhongliang, Mao, Richeng, and Zhang, Jiming

Subjects
ESTRADIOL benzoate, ESTROGEN receptors, ESTRADIOL, HEPATITIS B virus, LIFE cycles (Biology), TRANSPOSONS, HEPATITIS B, MOLECULES
Abstract

HBx plays a significant role in the cccDNA epigenetic modification regulating the hepatitis B virus (HBV) life cycle and in hepatocyte proliferation and carcinogenesis. By using the sleeping-beauty transposon system, we constructed a tetracycline-induced HBx-expressing stable cell line, SBHX21. HBx with a HiBiT tag can be quickly detected utilizing a NanoLuc-based HiBiT detection system. By screening a drug library using SBHX21 cells, we identified estradiol benzoate as a novel anti-HBx agent. Estradiol benzoate also markedly reduced the production of HBeAg, HBsAg, HBV pgRNA, and HBV DNA in a dose-dependent manner, suggesting that estradiol benzoate could be an anti-HBV agent. Docking model results revealed that estradiol benzoate binds to HBx at TRP87 and TRP107. Collectively, our results suggest that estradiol benzoate inhibits the HBx protein and HBV transcription and replication, which may serve as a novel anti-HBV molecular compound for investigating new treatment strategies for HBV infection. [ABSTRACT FROM AUTHOR]

Published
2022
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3. Quantitative Proteomic Analysis of Exosome Protein Content Changes Induced by Hepatitis B Virus in Huh-7 Cells Using SILAC Labeling and LC–MS/MS

Author

Xiaoxian Cui, Junqi Zhang, Lili Wei, Xue Zhao, Jing Liu, Xie Youhua, Jinlin Duan, Shen Zhongliang, Yanchun Ma, and Yanxin Wu

Subjects
Proteomics, Hepatitis B virus, Carcinoma, Hepatocellular, Proteome, viruses, Immunoblotting, Biology, Exosomes, Transfection, Virus Replication, medicine.disease_cause, Biochemistry, Exosome, Virus, Tandem Mass Spectrometry, Cell Line, Tumor, Stable isotope labeling by amino acids in cell culture, medicine, Humans, Replicon, Liver Neoplasms, virus diseases, General Chemistry, Molecular biology, digestive system diseases, Microvesicles, HBx, Isotope Labeling, Host-Pathogen Interactions, Chromatography, Liquid
Abstract

Hepatitis B virus (HBV) infection could cause hepatitis, liver cirrhosis, and hepatocellular carcinoma. HBV-mediated pathogenesis is only partially understood, but X protein (HBx) reportedly possesses oncogenic potential. Exosomes are small membrane vesicles with diverse functions released by various cells including hepatocytes, and HBV harnesses cellular exosome biogenesis and export machineries for virion morphogenesis and secretion. Therefore, HBV infection might cause changes in exosome contents with functional implications for both virus and host. In this work, exosome protein content changes induced by HBV and HBx were quantitatively analyzed by SILAC/LC-MS/MS. Exosomes prepared from SILAC-labeled hepatoma cell line Huh-7 transfected with HBx, wildtype, or HBx-null HBV replicon plasmids were analyzed by LC-MS/MS. Systematic analyses of MS data and confirmatory immunoblotting showed that HBx overexpression and HBV, with or without HBx, replication in Huh-7 cells indeed caused marked and specific changes in exosome protein contents. Furthermore, specific changes in protein contents were also detected in exosomes purified from HBV-infected patients' sera compared with control sera negative for HBV markers. These results illustrate a new aspect of interactions between HBV and the host and provide the foundation for future research into roles played by exosomes in HBV infection and pathogenesis.

Published
2014

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