ArticleMolecular biology reports2010
p53 Promotes proteasome-dependent degradation of oncogenic protein HBx by transcription of MDM2.
Article in Molecular biology reports, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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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
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- TP53 codon 72 polymorphism and colorectal cancer susceptibility: a meta-analysis.Molecular biology reports · 2011Pooled it
- Cooperation Between Aflatoxin-Induced p53 Aberrations and Hepatitis B Virus in Hepatocellular Carcinoma.Journal of xenobiotics · 2025Review
- An E3 ligase TRIM1 promotes colorectal cancer progression via K63-linked ubiquitination and activation of HIF1α.Oncogenesis · 2024Article
- JMJD2D stabilises and cooperates with HBx protein to promote HBV transcription and replication.JHEP reports : innovation in hepatology · 2023Article
- Role of Virally-Encoded Deubiquitinating Enzymes in Regulation of the Virus Life Cycle.International journal of molecular sciences · 2021Review
- The Hepatitis B Virus Interactome: A Comprehensive Overview.Frontiers in microbiology · 2021Review
- The role of MDM2-p53 axis dysfunction in the hepatocellular carcinoma transformation.Cell death discovery · 2020Review
- The interaction of hepatitis B virus with the ubiquitin proteasome system in viral replication and associated pathogenesis.Virology journal · 2019Review
- Chromatin remodelling factor BAF155 protects hepatitis B virus X protein (HBx) from ubiquitin-independent proteasomal degradation.Emerging microbes & infections · 2019Article
- Human Oncoviruses and p53 Tumor Suppressor Pathway Deregulation at the Origin of Human Cancers.Cancers · 2018Review
- MDM2-p53 Interactions in Human Hepatocellular Carcinoma: What Is the Role of Nutlins and New Therapeutic Options?Journal of clinical medicine · 2018Review
- Deubiquitylation of hepatitis B virus X protein (HBx) by ubiquitin-specific peptidase 15 (USP15) increases HBx stability and its transactivation activity.Scientific reports · 2017Article
- E3 Ubiquitin Ligase Siah-1 is Down-regulated and Fails to Target Natural HBx Truncates for Degradation in Hepatocellular Carcinoma.Journal of Cancer · 2016Article
- Molecular mechanism of hepatitis B virus X protein function in hepatocarcinogenesis.World journal of gastroenterology · 2015Review
- Liver-specific expressions of HBx and src in the p53 mutant trigger hepatocarcinogenesis in zebrafish.PloS one · 2013Article
- Hepatitis B virus X gene and hepatocarcinogenesis.Journal of gastroenterology · 2011Review
- The X-linked tumor suppressor TSPX interacts and promotes degradation of the hepatitis B viral protein HBx via the proteasome pathway.PloS one · 2011Article
- Interplay between MDM2, MDMX, Pirh2 and COP1: the negative regulators of p53.Molecular biology reports · 2011Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis B virus X protein (HBx) is closely involved in the development of hepatocellular carcinoma (HCC). Tumor suppressor p53 was reported to induce HBx degradation and repress its oncogenic function recently, but the molecular mechanism is unknown. In this study, we attempted to identify the underlying mechanism. We found that overexpression of p53 protein reduces the level of HBx protein and shortens its half-life, however, in MDM2 knock out cells, p53 has no effects on degradation of HBx, meanwhile, overexpression of MDM2 in absence of p53 can accelerate turnover of HBx protein. These indicate that p53-mediated HBx degradation is MDM2-dependent. MDM2 interacts with HBx in vitro and in vivo but does not promote its ubiquitination. In consistent with the results above, HCC tissue samples with wild-type p53 hardly detect HBx protein, whereas, HBx always accumulate in the tissues with mutant p53. Our data provide a possible mechanism on how p53 regulate HBx stability and also a new clue for the study of p53 mutation and HCC development.
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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.