ArticleOncotarget2016
Hepatitis B virus PreS2-mutant large surface antigen activates store-operated calcium entry and promotes chromosome instability.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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.
- Viral regulation of organelle membrane contact sites.PLoS biology · 2024Article
- Article
- State of the art treatment of hepatitis B virus hepatocellular carcinoma and the role of hepatitis B surface antigen post-liver transplantation and resection.Liver international : official journal of the International Association for the Study of the Liver · 2022Review
- Calcium signaling in hepatitis B virus infection and its potential as a therapeutic target.Cell communication and signaling : CCS · 2021Review
- Review
- Aerobic glycolysis supports hepatitis B virus protein synthesis through interaction between viral surface antigen and pyruvate kinase isoform M2.PLoS pathogens · 2021Article
- Hepatitis B Virus DNA Integration: In Vitro Models for Investigating Viral Pathogenesis and Persistence.Viruses · 2021Review
- Persistence of Hepatitis B Virus Infection: A Multi-Faceted Player for Hepatocarcinogenesis.Frontiers in microbiology · 2021Review
- A Rapid Immunochromatographic Method Based on a Secondary Antibody-Labelled Magnetic Nanoprobe for the Detection of Hepatitis B preS2 Surface Antigen.Biosensors · 2020Article
- The evolution and clinical impact of hepatitis B virus genome diversity.Nature reviews. Gastroenterology & hepatology · 2020Review
- Effect of Hepatitis Viruses on the Nrf2/Keap1-Signaling Pathway and Its Impact on Viral Replication and Pathogenesis.International journal of molecular sciences · 2019Review
- Review
- Structure-Guided Approach to Identify Potential Inhibitors of Large Envelope Protein to Prevent Hepatitis B Virus Infection.Oxidative medicine and cellular longevity · 2019Article
- Liver regeneration accelerates hepatitis B virus-related tumorigenesis of hepatocellular carcinoma.Molecular oncology · 2018Article
- Hepatitis B Virus X Protein Upregulates Intracellular Calcium Signaling by Binding C-terminal of Orail Protein.Current medical science · 2018Article
- Expression of hepatitis B virus surface antigens induces defective gonad phenotypes in Caenorhabditis elegans.World journal of virology · 2017Article
- Zika virus causes supernumerary foci with centriolar proteins and impaired spindle positioning.Open biology · 2017Article
- Molecular Mechanisms and Therapeutic Targets of Hepatitis B Virus Pre-S Mutant-Associated Hepatocellular Carcinoma Tumorigenesis.Cancer control : journal of the Moffitt Cancer CenterReview
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis B virus (HBV) is a driver of hepatocellular carcinoma, and two viral products, X and large surface antigen (LHBS), are viral oncoproteins. During chronic viral infection, immune-escape mutants on the preS2 region of LHBS (preS2-LHBS) are gain-of-function mutations that are linked to preneoplastic ground glass hepatocytes (GGHs) and early disease onset of hepatocellular carcinoma. Here, we show that preS2-LHBS provoked calcium release from the endoplasmic reticulum (ER) and triggered stored-operated calcium entry (SOCE). The activation of SOCE increased ER and plasma membrane (PM) connections, which was linked by ER- resident stromal interaction molecule-1 (STIM1) protein and PM-resident calcium release- activated calcium modulator 1 (Orai1). Persistent activation of SOCE induced centrosome overduplication, aberrant multipolar division, chromosome aneuploidy, anchorage-independent growth, and xenograft tumorigenesis in hepatocytes expressing preS2- LHBS. Chemical inhibitions of SOCE machinery and silencing of STIM1 significantly reduced centrosome numbers, multipolar division, and xenograft tumorigenesis induced by preS2-LHBS. These results provide the first mechanistic link between calcium homeostasis and chromosome instability in hepatocytes carrying preS2-LHBS. Therefore, persistent activation of SOCE represents a novel pathological mechanism in HBV-mediated hepatocarcinogenesis.
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