ArticleHepatology (Baltimore, Md.)2011
Modeling hepatitis B virus X-induced hepatocellular carcinoma in mice with the Sleeping Beauty transposon system.
Article in Hepatology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 76 citations in OpenAlex.
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- Mechanisms of hepatocellular carcinoma and cirrhosis development in concurrent steatotic liver disease and chronic hepatitis B.Clinical and molecular hepatology · 2025Review
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- Arginine methylation of HSPA8 by PRMT9 inhibits ferroptosis to accelerate hepatitis B virus-associated hepatocellular carcinoma progression.Journal of translational medicine · 2023Article
- The Conserved LncRNA DIO3OS Restricts Hepatocellular Carcinoma Stemness by Interfering with NONO-Mediated Nuclear Export of ZEB1 mRNA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Article
- DNA Deamination Is Required for Human APOBEC3A-Driven Hepatocellular Carcinoma In Vivo.International journal of molecular sciences · 2023Article
- Role of hepatitis B virus in development of hepatocellular carcinoma: Focus on covalently closed circular DNA.World journal of hepatology · 2022Review
- Cellular origins of regenerating liver and hepatocellular carcinoma.JHEP reports : innovation in hepatology · 2022Review
- Molecular Mechanisms and Animal Models of HBV-Related Hepatocellular Carcinoma: With Emphasis on Metastatic Tumor Antigen 1.International journal of molecular sciences · 2021Review
- MAPK/ERK Signaling Pathway in Hepatocellular Carcinoma.Cancers · 2021Review
- ZBTB20 regulates WNT/CTNNB1 signalling pathway by suppressing PPARG during hepatocellular carcinoma tumourigenesis.JHEP reports : innovation in hepatology · 2021Article
- C-terminal truncated HBx initiates hepatocarcinogenesis by downregulating TXNIP and reprogramming glucose metabolism.Oncogene · 2021Article
- APOBEC3A catalyzes mutation and drives carcinogenesis in vivo.The Journal of experimental medicine · 2020Article
- Review
- R-spondin 2 Drives Liver Tumor Development in a Yes-Associated Protein-Dependent Manner.Hepatology communications · 2019Article
- HBx-K130M/V131I Promotes Liver Cancer in Transgenic Mice via AKT/FOXO1 Signaling Pathway and Arachidonic Acid Metabolism.Molecular cancer research : MCR · 2019Article
- Molecular Mechanisms Driving Progression of Liver Cirrhosis towards Hepatocellular Carcinoma in Chronic Hepatitis B and C Infections: A Review.International journal of molecular sciences · 2019Review
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledThe mechanisms associated with hepatitis B virus (HBV)-induced hepatocellular carcinoma (HCC) remain elusive, and there are currently no well-established animal models for studying this disease. Using the Sleeping Beauty transposon as a delivery system, we introduced an oncogenic component of HBV, the hepatitis B virus X (HBx) gene, into the livers of fumarylacetoacetate hydrolase (Fah) mutant mice via hydrodynamic tail vein injections. Coexpression of Fah complementary DNA from the transposon vector allowed for the selective repopulation of genetically corrected hepatocytes in Fah mutant mice. The process of hydrodynamic delivery induced liver inflammation, and the subsequent selective repopulation of hepatocytes carrying the transgene(s) could provide useful genetic information about the mechanisms of HBV-induced hyperplasia. Short hairpin RNA directed against transformation-related protein 53 (shp53) or other tumor suppressor genes and oncogenes [e.g., constitutively active neuroblastoma RAS viral (v-ras) oncogene homolog with Gly12Val substitution (NRAS(G12V) )] could also be codelivered with HBx by this system so that we could determine whether oncogenic cooperation existed. We found that the expression of HBx induced the activation of β-catenin expression in hydrodynamically injected livers, and this indicated its association with the Wnt signaling pathway in HBV-induced hyperplasia. HBx coinjected with shp53 accelerated the formation of liver hyperplasia in these mice. As expected, constitutively active NRAS(G12V) alone was sufficient to induce liver hyperplasia, and its tumorigenicity was augmented when it was coinjected with shp53. Interestingly, HBx did not seem to cooperate with constitutively active NRAS(G12V) in driving liver tumorigenesis.
conclusionThis system can be used as a model for studying the various genetic contributions of HBV to liver hyperplasia and finally HCC in an in vivo system.
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