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HBV Upregulates CtBP2 Expression via the X Gene
Xinghui Liu1, Chengliang Zhu2, Jie Li1
1Department of Clinical Laboratory, Shanghai Gongli Hospital, The Second Military Medical University, Pudong New Area, Shanghai 200135, China.
Biomed Research International
|August 29, 2018
Summary
Hepatitis B virus (HBV) infection increases the expression of Carboxyl-terminal-binding protein 2 (CtBP2), a key factor in tumor development. This suggests HBV may promote liver cancer by upregulating CtBP2.
Area of Science:
- Hepatology
- Oncology
- Molecular Biology
Background:
- Hepatitis B virus (HBV) infection is a major cause of liver disease, including cirrhosis and hepatocellular carcinoma (HCC).
- The precise mechanisms of HBV-induced carcinogenesis are not fully elucidated.
- Carboxyl-terminal-binding protein 2 (CtBP2) is implicated in tumor progression and tumorigenesis.
Purpose of the Study:
- To investigate the impact of HBV infection on CtBP2 expression.
- To explore the underlying molecular mechanisms by which HBV influences CtBP2.
Main Methods:
- Quantitative reverse transcription polymerase chain reaction (RT-qPCR) and western blotting were employed to measure CtBP2 mRNA and protein levels.
- HepG2 cells were transfected with an HBV infectious clone (pHBV1.3) and HBV gene expression plasmids.
- Luciferase reporter assays were used to assess the effect of HBV components on the CtBP2 gene promoter activity.
Main Results:
- CtBP2 expression was elevated in HBV-associated HCC tissues compared to adjacent non-cancerous tissues.
- HBV integration and expression in HepG2 cells led to increased CtBP2 mRNA and protein levels.
- The HBV X gene significantly activated the CtBP2 promoter and upregulated CtBP2 expression in a dose-dependent manner.
Conclusions:
- HBV infection may contribute to the development and progression of HCC.
- Upregulation of CtBP2 expression by HBV, particularly the X gene, is a potential mechanism driving hepatocarcinogenesis.
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