ArticleVirology journal2018
The truncated mutant HBsAg expression increases the tumorigenesis of hepatitis B virus by regulating TGF-β/Smad signaling pathway.
Article in Virology journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- The relationship between mutations in reverse transcriptase region of hepatitis B virus and progression of liver disease.Virus genes · 2026Article
- Multiplex gene editing suppresses random integration of hepatitis B virus DNA in chronically infected liver.Molecular therapy. Nucleic acids · 2026Article
- The APOBEC3 family: a narrative review of an alternative therapeutic agent for hepatitis B virus-induced hepatocellular carcinoma.Journal of gastrointestinal oncology · 2026Review
- Review
- Review
- The impact of integrated hepatitis B virus DNA on oncogenesis and antiviral therapy.Biomarker research · 2024Review
- Mangiferin for the Management of Liver Diseases: A Review.Foods (Basel, Switzerland) · 2023Review
- Hepatitis B Virus-Encoded MicroRNA (HBV-miR-3) Inhibits FIH-1 Expression to Promote Tumor Angiogenesis in HBV-Related Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2023Article
- Endemic HBV among hospital in-patients in Bangladesh, including evidence of occult infection.The Journal of general virology · 2021Article
- Hepatitis B Virus preS/S Truncation Mutant rtM204I/sW196* Increases Carcinogenesis through DeregulatedInternational journal of molecular sciences · 2020Article
- 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
- A putative hepatitis B virus sequence motif associated with hepatocellular carcinoma in South African adults.Annals of hepatologyArticle
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Authors and funding
7 authors.
Funding
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Abstract
backgroundIt has been reported that the emergence of HBV rtA181T/sW172* mutant could result in a dominant secretion defect of HBsAg and increase the risk of HCC development. This study was designed to reveal the role and possible pathogenic mechanism of truncated mutant HBsAg in tumorigenesis of HBV rtA181T/sW172* mutant.
resultsAs compared to wide type or substituted mutant HBsAg, the ratio of cell clones was significant higher in L02 cells stable expressing truncated mutant HBsAg. Injection of L02 cells stable expressing truncated mutant HBsAg into the dorsal skin fold of nude mice resulted in increased primary tumor growth compared to L02 cells stable expressing wide-type and substituted mutant HBsAg. In HBV replication L02 cell lines, the key molecular involved in TGF-β/Smad pathway was also investigated. We found that the mRNA and protein levels of Smad3/2, CREB and CyclinD1 were significantly higher and TGFBI level was significantly lower in cells stably expressing truncated mutant HBsAg as compared to cells stably expressing wide-type and substituted mutant HBsAg. Additionally, after administration of TGF-β1 (increasing TGFBI level), the volume of tumor is obviously reduced in nude mice with injection of L02 cells stable expressing truncated HBsAg.
conclusionsThe emergence of sW172* mutant may increase the tumorigenesis of HBV, and its mechanism may be associated with down-regulated expression of TGFBI in TGF-β/Smad signaling pathway.
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