ArticleOncogene2001
Hepatitis B virus X mutants derived from human hepatocellular carcinoma retain the ability to abrogate p53-induced apoptosis.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed, 91 citations in OpenAlex.
- HBV DNA integration gene CCDC91 is oncogenic and a potential therapeutic target for hepatocellular carcinoma.Communications biology · 2025Article
- Pathogenesis of Hepatocellular Carcinoma: The Interplay of Apoptosis and Autophagy.Biomedicines · 2023Review
- Implications of Possible HBV-Driven Regulation of Gene Expression in Stem Cell-like Subpopulation of Huh-7 Hepatocellular Carcinoma Cell Line.Journal of personalized medicine · 2022Article
- Hepatocellular Carcinoma in Chronic Viral Hepatitis: Where Do We Stand?International journal of molecular sciences · 2022Review
- Review
- Roles of p53 in extrinsic factor-induced liver carcinogenesis.Hepatoma research · 2017Article
- Transposon mouse models to elucidate the genetic mechanisms of hepatitis B viral induced hepatocellular carcinoma.World journal of gastroenterology · 2015Review
- Immune-mediated Liver Injury in Hepatitis B Virus Infection.Immune network · 2015Review
- Somatic mutations, viral integration and epigenetic modification in the evolution of hepatitis B virus-induced hepatocellular carcinoma.Current genomics · 2014Article
- Identification of two novel functional p53 responsive elements in the herpes simplex virus-1 genome.Virology · 2014Article
- Modulation of the unfolded protein response by the human hepatitis B virus.Frontiers in microbiology · 2014Review
- Hepatitis B virus X (HBx) play an anti-apoptosis role in hepatic progenitor cells by activating Wnt/β-catenin pathway.Molecular and cellular biochemistry · 2013Article
- Show me your license, please: deregulation of centriole duplication mechanisms that promote amplification.Cellular and molecular life sciences : CMLS · 2013Review
- Modeling hepatitis B virus X-induced hepatocellular carcinoma in mice with the Sleeping Beauty transposon system.Hepatology (Baltimore, Md.) · 2011Article
- Tumor initiation and progression in hepatocellular carcinoma: risk factors, classification, and therapeutic targets.Acta pharmacologica Sinica · 2010Review
- Apoptosis of hepatitis B virus-infected hepatocytes prevents release of infectious virus.Journal of virology · 2010Article
- Cooperation of tumor-derived HBx mutants and p53-249(ser) mutant in regulating cell proliferation, anchorage-independent growth and aneuploidy in a telomerase-immortalized normal human hepatocyte-derived cell line.International journal of cancer · 2010Article
- Occult hepatitis B virus infection in ART-naive HIV-infected patients seen at a tertiary care centre in north India.BMC infectious diseases · 2010Article
- Article
- TP53 mutations and hepatocellular carcinoma: insights into the etiology and pathogenesis of liver cancer.Oncogene · 2007Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic hepatitis B virus (HBV) infection and the integration of its X gene (HBx) are closely associated with the development of hepatocellular carcinoma (HCC). The integrated HBx frequently is truncated or contains point mutations. Previous studies indicated that these HBx mutants have a diminished co-transactivational activity. We have compared the effects of wild-type (wt) HBx and its naturally occurring mutants derived from human HCCs on transcriptional co-transactivation, apoptosis and interactive effects with p53. We demonstrated that overexpression of mutant, but not wt HBx, is defective in transcriptional co-transactivation of the NF-kappaB-driven luciferase reporter. By using a microinjection technique, the HBx mutants were shown to have an attenuated pro-apoptotic activity. This deficiency may be attributed to multiple mutations in the co-transactivation domain of HBx, that leads to decreased stability of the translated product. However, wt or mutant HBx bind to p53 in vitro and retain their ability to block p53-mediated apoptosis in vivo, which has been implicated as its major tumor suppressor function. The abrogation of p53-mediated apoptosis by integrated HBx mutants may provide a selective clonal advantage for preneoplastic or neoplastic hepatocytes and contribute to hepatocellular carcinogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.