ArticleCell death and differentiation2016
The transcription factor c-JUN/AP-1 promotes HBV-related liver tumorigenesis in mice.
Article in Cell death and differentiation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 66 citations in OpenAlex.
- Chromatin remodeler BAF maintains HBV cccDNA transcriptional competence and represents a therapeutic target.Nucleic acids research · 2026Article
- Pharmacological Inhibition of c-Jun N-Terminal Kinase Activity Exacerbates Liver Damage in Schistosoma mansoni Infected Mice.Liver international : official journal of the International Association for the Study of the Liver · 2025Article
- Multi-omics analysis reveals distinct gene regulatory mechanisms between primary and organoid-derived human hepatocytes.Disease models & mechanisms · 2025Article
- Liver cancer development driven by the AP-1/c-Jun~Fra-2 dimer through c-Myc.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Mitochondria-mediated ferroptosis induced by CARD9 ablation prevents MDSCs-dependent antifungal immunity.Cell communication and signaling : CCS · 2024Article
- PTEN deficiency potentiates HBV-associated liver cancer development through augmented GP73/GOLM1.Journal of translational medicine · 2024Article
- Hepatocyte integrity depends on c-Jun-controlled proliferation in Schistosoma mansoni infected mice.Scientific reports · 2023Article
- Review
- Detecting Liver Cancer Using Cell-Free DNA Fragmentomes.Cancer discovery · 2023Article
- Drug Screening for Hepatitis A Virus (HAV): Nicotinamide Inhibits c-Jun Expression and HAV Replication.Journal of virology · 2023Article
- Key genes associated with non-alcoholic fatty liver disease and hepatocellular carcinoma with metabolic risk factors.Frontiers in genetics · 2023Article
- Specific gut microbiome signature predicts hepatitis B virus-related hepatocellular carcinoma patients with microvascular invasion.Annals of medicine · 2023Article
- 2,3,4',5‑Tetrahydroxystilbene‑2‑O‑β‑D‑glucoside ameliorates gentamicin‑induced ototoxicity by modulating autophagy via Sesn2/AMPK/mTOR signaling.International journal of molecular medicine · 2022Article
- N-n-Butyl haloperidol iodide ameliorates liver fibrosis and hepatic stellate cell activation in mice.Acta pharmacologica Sinica · 2022Article
- Probing Synergistic Targets by Natural Compounds for Hepatocellular Carcinoma.Frontiers in cell and developmental biology · 2021Article
- A saturated fatty acid-rich diet enhances hepatic lipogenesis and tumorigenesis in HCV core gene transgenic mice.The Journal of nutritional biochemistry · 2020Article
- Review
- Single-Cell RNA-Seq Analysis Reveals Microenvironmental Infiltration of Plasma Cells and Hepatocytic Prognostic Markers in HCC With Cirrhosis.Frontiers in oncology · 2020Article
- Elevated double-strand break repair protein RAD50 predicts poor prognosis in hepatitis B virus-related hepatocellular carcinoma: A study based on Chinese high-risk cohorts.Journal of Cancer · 2020Article
- Network Pharmacology-Based Study on the Mechanism ofEvidence-based complementary and alternative medicine : eCAM · 2020Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) develops as a consequence of chronic inflammatory liver diseases such as chronic hepatitis B virus (HBV) infection. The transcription factor c-Jun/activator protein 1 (AP-1) is strongly expressed in response to inflammatory stimuli, promotes hepatocyte survival during acute hepatitis and acts as an oncogene during chemically induced liver carcinogenesis in mice. Here, we therefore aimed to characterize the functions of c-Jun during HBV-related liver tumorigenesis. To this end, transgenic mice expressing all HBV envelope proteins (HBV(+)), an established model of HBV-related HCC, were crossed with knockout mice lacking c-Jun specifically in hepatocytes and tumorigenesis was analyzed. Hepatic expression of c-Jun was strongly induced at several time points during tumorigenesis in HBV(+) mice, whereas expression of other AP-1 components remained unchanged. Importantly, formation of premalignant foci and tumors was strongly reduced in HBV(+) mice lacking c-Jun. This phenotype correlated with impaired hepatocyte proliferation and increased expression of the cell cycle inhibitor p21, whereas hepatocyte survival was not affected. Progression and prognosis of HBV-related HCC correlates with the expression of the cytokine osteopontin (Opn), an established AP-1 target gene. Opn expression was strongly reduced in HBV(+) livers and primary mouse hepatocytes lacking c-Jun, demonstrating that c-Jun regulates hepatic Opn expression in a cell-autonomous manner. These findings indicate that c-Jun has important functions during HBV-associated tumorigenesis by promoting hepatocyte proliferation as well as progression of dysplasia. Therefore, targeting c-Jun may be a useful strategy to prevent hepatitis-associated tumorigenesis.
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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.