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09:02
Modeling Hepatitis B Virus Infection in Non-Hepatic 293T-NE-3NRs Cells
Published on: June 5, 2020
[Hepatitis B virus and hepatocellular carcinoma]
P Tiollais1, A Dejean, M A Buendia
1Unité de recombinaison et expression génétique, INSERM U. 163, Institut Pasteur, Paris.
Annales De Gastroenterologie Et D'Hepatologie
|November 1, 1991
Summary
Woodchuck hepatitis virus and hepatitis B virus (HBV) can cause liver cancer. Viral DNA integration near proto-oncogenes like c-myc or retinoic acid receptors can lead to tumor development through insertional mutagenesis.
Area of Science:
- Hepatology
- Oncology
- Molecular Biology
Background:
- Hepatocellular carcinoma (HCC) is a major global health concern.
- The role of viral hepatitis in liver carcinogenesis is well-established.
- Mechanisms of viral-induced oncogenesis, including insertional mutagenesis, require further elucidation.
Purpose of the Study:
- To investigate the role of woodchuck hepatitis virus (WHV) and hepatitis B virus (HBV) integration in liver tumor development.
- To characterize the molecular events associated with viral DNA integration near proto-oncogenes.
- To explore the potential of insertional mutagenesis as a mechanism in viral hepatitis-related liver cancer.
Main Methods:
- Analysis of WHV integration sites in woodchuck hepatocellular carcinoma.
- Molecular characterization of viral-host DNA junctions and gene expression.
- Comparison of HBV integration sites in human hepatoma with normal tissue.
Main Results:
- WHV integration near the c-myc oncogene in woodchuck tumors led to overexpression of c-myc or its transcripts.
- HBV DNA insertion in a human hepatoma occurred within a putative exon similar to thyroid/steroid hormone receptors.
- This HBV insertion resulted in the inappropriate expression of a chimeric retinoic acid receptor gene (hap gene).
Conclusions:
- Viral integration near proto-oncogenes can contribute to liver tumor initiation.
- HBV may play a direct role in liver carcinogenesis through insertional mutagenesis.
- These findings highlight the potential for viral DNA to disrupt cellular genes, promoting cancer development.
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