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Utilizing Experimental Mouse Model to Identify Effectors of Hepatocellular Carcinoma Induced by HBx Antigen

Overview
Journal Cancers (Basel)
Publisher MDPI
Specialty Oncology
Date 2020 Feb 14
PMID 32050622
Citations 8
Authors
Affiliations
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Abstract

Hepatocellular carcinoma (HCC) is among the ten most commonly diagnosed cancers and the fourth leading cause of cancer-related death. Patients with hepatitis B virus (HBV) infection are prone to developing chronic liver diseases (i.e., fibrosis and cirrhosis), and the HBV X antigen plays an important role in the development of HCC. The difficulty in detecting HCC at the early stages is one of the main reasons that the death rate approximates the incidence rate. The regulators controlling the downstream liver protein expression from HBV infection are unclear. Mass spectrometric techniques and customized programs were used to identify differentially expressed proteins which may be involved in the development of liver fibrosis and HCC progression in hepatitis B virus X protein transgenic mice (HBx mice). FSTL1, CTSB, and TGF-β enhanced the signaling pathway proteins during the pathogenesis of HBx. Missing proteins can be essential in cell growth, differentiation, apoptosis, migration, metastasis or angiogenesis. We found that LHX2, BMP-5 and GDF11 had complex interactions with other missing proteins and BMP-5 had both tumor suppressing and tumorigenic roles. BMP-5 may be involved in fibrosis and tumorigenic processes in the liver. These results provide us an understanding of the mechanism of HBx-induced disorders, and may serve as molecular targets for liver treatment.

Citing Articles

Hepatitis B virus X protein and TGF-β: partners in the carcinogenic journey of hepatocellular carcinoma.

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GDF11: An emerging therapeutic target for liver diseases and fibrosis.

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Hepatitis B x (HBx) as a Component of a Functional Cure for Chronic Hepatitis B.

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FSTL1-USP10-Notch1 Signaling Axis Protects Against Cardiac Dysfunction Through Inhibition of Myocardial Fibrosis in Diabetic Mice.

Lu L, Ma J, Liu Y, Shao Y, Xiong X, Duan W Front Cell Dev Biol. 2021; 9:757068.

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HBV HBx-Downregulated lncRNA Attenuates Cell Proliferation by Interacting with Vimentin.

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