Gene modulation associated with inhibition of liver regeneration in hepatitis B virus X transgenic mice

Sidorkiewicz, M; Jaı̈s, Jean-Philippe; Tralhao, Guilherme; Morosan, Serban; Giannini, Carlo; Brezillon, Nicolas; Soussan, Patrick Ben; Delpuech, Oona; Kremsdorf, Dina

doi:10.3748/wjg.14.574

Cited by 8 publications

(5 citation statements)

References 48 publications

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“…Previous investigations revealed that a number of cellular genes could be downregulated or upregulated by HBx, as indicated by oligonucleotide microarray analysis [12][13][14], which is difficult to be elucidated by the known genetic regulators. Interestingly, several studies have reported a strong correlation between HBV infection and epigenetic alteration of tumor suppressor genes, including p16 [15] and GSPT1 [16], whose expression is frequently downregulated in HCC by hypermethylation.…”

Section: Introductionmentioning

confidence: 98%

Epigenetic modification induced by hepatitis B virus X protein via interaction with de novo DNA methyltransferase DNMT3A

Zheng

Zhang

Cheng

et al. 2009

Journal of Hepatology

172

165

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Section: Introductionmentioning

confidence: 98%

Epigenetic modification induced by hepatitis B virus X protein via interaction with de novo DNA methyltransferase DNMT3A

Zheng

Zhang

Cheng

et al. 2009

Journal of Hepatology

172

165

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“…As outlined above, HBx could block apoptosis in CLD and via activation of NF-κB. In contrast, when HBx is expressed in normal mouse liver, and such mice are subjected to partial hepatectomy, liver regeneration is largely inhibited [ 58 ]. In the latter case, the levels of free radicals, and corresponding HBx expression and activity are low.…”

Section: Introductionmentioning

confidence: 99%

Hepatitis B x antigen (HBx) is an important therapeutic target in the pathogenesis of hepatocellular carcinoma

2021

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Hepatitis B virus (HBV) is a human pathogen that has infected an estimated two billion people worldwide. Despite the availability of highly efficacious vaccines, universal screening of the blood supply for virus, and potent direct acting antiviral drugs, there are more than 250 million carriers of HBV who are at risk for the sequential development of hepatitis, fibrosis, cirrhosis and hepatocellular carcinoma (HCC). More than 800,000 deaths per year are attributed to chronic hepatitis B. Many different therapeutic approaches have been developed to block virus replication, and although effective, none are curative. These treatments have little or no impact upon the portions of integrated HBV DNA, which often encode the virus regulatory protein, HBx. Although given little attention, HBx is an important therapeutic target because it contributes importantly to (a) HBV replication, (b) in protecting infected cells from immune mediated destruction during chronic infection, and (c) in the development of HCC. Thus, the development of therapies targeting HBx, combined with other established therapies, will provide a functional cure that will target virus replication and further reduce or eliminate both the morbidity and mortality associated with chronic liver disease and HCC. Simultaneous targeting of all these characteristics underscores the importance of developing therapies against HBx.

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Section: Hbv Infection and Liver Regenerationmentioning

confidence: 99%

“…The effect of HBx on the gene expression profile in the regenerated liver after partial hepatectomy of HBx-transgenic mice has been analyzed [ 65 ]. Impaired DNA synthesis and reduction in liver mass in HBx-transgenic mice have been shown to be associated with a weaker expression of genes involved in the cholesterol and nonsterol isoprenoid pathways, as well as serum amyloid A [ 65 ]. Moreover, using MALDI imaging MS analysis, we have previously reported that phosphatidylcholine biosynthesis in the regenerating liver is altered by HBV infection, causing a regeneration defect [ 63 ].…”

Section: Hbv Infection and Liver Regenerationmentioning

confidence: 99%

Dysregulation of Liver Regeneration by Hepatitis B Virus Infection: Impact on Development of Hepatocellular Carcinoma

Park

Dezhbord

Lee

et al. 2022

Cancers

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The liver is unique in its ability to regenerate in response to damage. The complex process of liver regeneration consists of multiple interactive pathways. About 2 billion people worldwide have been infected with hepatitis B virus (HBV), and HBV causes 686,000 deaths each year due to its complications. Long-term infection with HBV, which causes chronic inflammation, leads to serious liver-related diseases, including cirrhosis and hepatocellular carcinoma. HBV infection has been reported to interfere with the critical mechanisms required for liver regeneration. In this review, the studies on liver tissue characteristics and liver regeneration mechanisms are summarized. Moreover, the inhibitory mechanisms of HBV infection in liver regeneration are investigated. Finally, the association between interrupted liver regeneration and hepatocarcinogenesis, which are both triggered by HBV infection, is outlined. Understanding the fundamental and complex liver regeneration process is expected to provide significant therapeutic advantages for HBV-associated hepatocellular carcinoma.

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Gene modulation associated with inhibition of liver regeneration in hepatitis B virus X transgenic mice

Abstract: biosynthesis (farnesyl diphosphate synthase, Cyp7b1, geranylgeranyl diphosphate synthase, SAA3). CONCLUSION:Our results provide a novel insight into the biological activities of HBx, implicated in the inhibition of liver regeneration.

Cited by 8 publications

References 48 publications

Epigenetic modification induced by hepatitis B virus X protein via interaction with de novo DNA methyltransferase DNMT3A

Epigenetic modification induced by hepatitis B virus X protein via interaction with de novo DNA methyltransferase DNMT3A

Hepatitis B x antigen (HBx) is an important therapeutic target in the pathogenesis of hepatocellular carcinoma

Dysregulation of Liver Regeneration by Hepatitis B Virus Infection: Impact on Development of Hepatocellular Carcinoma

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