ArticleJournal of clinical and translational hepatology2021
Interaction of Hepatitis B Virus X Protein with the Pregnane X Receptor Enhances the Synergistic Effects of Aflatoxin B1 and Hepatitis B Virus on Promoting Hepatocarcinogenesis.
Article in Journal of clinical and translational hepatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Peroxiredoxin II as a metabolic gatekeeper against aflatoxin BMycotoxin research · 2026Article
- Aflatoxin-associated hepatocarcinogenesis in a changing climate: the gut microbiome as a missing link in the One Health framework.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Hepatitis B virus protein X promotes survival and loss of hepatocyte identity in a differentiated human liver organoid system.Cell death and differentiation · 2026Article
- A six-gene prognostic signature for aflatoxin B1-associated hepatocellular carcinoma identified through integrated bioinformatics and network toxicology.Translational gastroenterology and hepatology · 2026Article
- Mechanistic interplay between aflatoxin B1 and tissue inhibitor of metalloproteinase-3 in hepatocellular carcinoma.World journal of hepatology · 2025Article
- Comprehensive review for aflatoxin detoxification with special attention to cold plasma treatment.Mycotoxin research · 2025Review
- Role of the Synergistic Interactions of Environmental Pollutants in the Development of Cancer.GeoHealth · 2022Review
- Regulation of PXR Function by Coactivator and Corepressor Proteins: Ligand Binding Is Just the Beginning.Cells · 2021Review
- Article
- Advances in the treatment of hepatocellular carcinoma: An overview of the current and evolving therapeutic landscape for clinicians.CA: a cancer journal for cliniciansReview
Corrections and comments
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Authors and funding
8 authors at 7 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimsHepatitis B virus (HBV) infection has been found to increase hepatocellular sensitivity to carcinogenic xenobiotics, by unknown mechanisms, in the generation of hepatocellular carcinoma. The pregnane X receptor (PXR) is a key regulator of the body's defense against xenobiotics, including xenobiotic carcinogens and clinical drugs. In this study, we aimed to investigate the molecular mechanisms of HBV X protein (HBx)-PXR signaling in the synergistic effects of chemical carcinogens in HBV-associated hepatocarcinogenesis.
methodsThe expression profile of PXR-cytochrome p450 3A4 (CYP3A4) signaling was determined by PCR, western blotting, and tissue microarray. Cell viability and aflatoxin B1 (AFB1) cytotoxicity were measured using the cell counting kit-8 assay. Target gene expression was evaluated using transient transfection and real time-PCR. The genotoxicity of AFB1 was assessed in newborn mice with a single dose of AFB1.
resultsHBx enhanced the hepatotoxicity of AFB1 by activating CYP3A4 and reducing glutathione S-transferase Mu 1 (GSTM1) in cell lines. Activation of PXR by pregnenolone 16α-carbonitrile increased AFB1-induced liver tumor incidence by up-regulating oncogenic KRAS to enhance interleukin (IL)-11:IL-11 receptor subunit alpha-1 (IL11RA-1)-mediated inflammation in an HBx transgenic model.
conclusionsOur finding regarding AFB1 toxicity enhancement by an HBx-PXR-CYP3A4/ GSTM1-KRAS-IL11:IL11RA signaling axis provides a rational explanation for the synergistic effects of chemical carcinogens in HBV infection-associated hepatocarcinogenesis.
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