ArticleCancer prevention research (Philadelphia, Pa.)2014
Alcohol consumption promotes diethylnitrosamine-induced hepatocarcinogenesis in male mice through activation of the Wnt/β-catenin signaling pathway.
Article in Cancer prevention research (Philadelphia, Pa.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Alcohol-Associated Hepatocarcinogenesis: Wnt/β-Catenin in Action.The American journal of pathology · 2026Pooled it
- Multiomics characterization of an alcohol-induced hepatocellular carcinoma mouse model.Lab animal · 2026Article
- Navigating liver cancer with mouse models: a comprehensive overview of HCC experimental systems.Journal of liver cancer · 2025Article
- Oncogenic plasmid DNA and liver injury agent dictates liver cancer development in a mouse model.Clinical science (London, England : 1979) · 2024Article
- Advances in the Pathogenesis of Metabolic Liver Disease-Related Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2024Review
- MiRNAs in Alcohol-Related Liver Diseases and Hepatocellular Carcinoma: A Step toward New Therapeutic Approaches?Cancers · 2023Review
- Retinoids in the Pathogenesis and Treatment of Liver Diseases.Nutrients · 2022Review
- Acute Intoxication With Alcohol Reduces Trauma-Induced Proinflammatory Response and Barrier Breakdown in the LungFrontiers in immunology · 2022Article
- In Vivo and In Vitro Models of Hepatocellular Carcinoma: Current Strategies for Translational Modeling.Cancers · 2021Review
- Potential role of gut microbiota, the proto-oncogene PIKE (Agap2) and cytochrome P450 CYP2W1 in promotion of liver cancer by alcoholic and nonalcoholic fatty liver disease and protection by dietary soy protein.Chemico-biological interactions · 2020Article
- Hepatocellular Protein Arginine Methyltransferase 1 Suppresses Alcohol-Induced Hepatocellular Carcinoma Formation by Inhibition of Inducible Nitric Oxide Synthase.Hepatology communications · 2020Article
- Curcumin- and Cyclopamine-Loaded Liposomes to Enhance Therapeutic Efficacy Against Hepatic Fibrosis.Drug design, development and therapy · 2020Article
- Prospects and Perspectives for WISP1 (CCN4) in Diabetes Mellitus.Current neurovascular research · 2020Review
- PRMT1-Dependent Macrophage IL-6 Production Is Required for Alcohol-Induced HCC Progression.Gene expression · 2019Article
- Protein arginine methyl transferase 1- and Jumonji C domain-containing protein 6-dependent arginine methylation regulate hepatocyte nuclear factor 4 alpha expression and hepatocyte proliferation in mice.Hepatology (Baltimore, Md.) · 2018Article
- Pre-clinical and clinical investigations of metabolic zonation in liver diseases: The potential of microphysiology systems.Experimental biology and medicine (Maywood, N.J.) · 2017Review
- The in vivo antineoplastic and therapeutic efficacy of troxerutin on rat preneoplastic liver: biochemical, histological and cellular aspects.European journal of nutrition · 2017Article
- Soy protein isolate inhibits hepatic tumor promotion in mice fed a high-fat liquid diet.Experimental biology and medicine (Maywood, N.J.) · 2017Article
- Article
- Role of cytokines and chemokines in alcohol-induced tumor promotion.OncoTargets and therapy · 2017Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Although alcohol effects within the liver have been extensively studied, the complex mechanisms by which alcohol causes liver cancer are not well understood. It has been suggested that ethanol (EtOH) metabolism promotes tumor growth by increasing hepatocyte proliferation. In this study, we developed a mouse model of tumor promotion by chronic EtOH consumption in which EtOH feeding began 46 days after injection of the chemical carcinogen diethylnitrosamine (DEN) and continued for 16 weeks. With a final EtOH concentration of 28% of total calories, we observed a significant increase in the total number of preneoplastic foci and liver tumors per mouse in the EtOH+DEN group compared with corresponding pair-fed (PF)+DEN and chow+DEN control groups. We also observed a 4-fold increase in hepatocyte proliferation (P < 0.05) and increased cytoplasmic staining of active-β-catenin in nontumor liver sections from EtOH+DEN mice compared with PF+DEN controls. In a rat model of alcohol-induced liver disease, we found increased hepatocyte proliferation (P < 0.05); depletion of retinol and retinoic acid stores (P < 0.05); increased expression of cytosolic and nuclear expression of β-catenin (P < 0.05) and phosphorylated-glycogen synthase kinase 3β (p-GSK3β), P < 0.05; significant upregulation in Wnt7a mRNA expression; and increased expression of several β-catenin targets, including, glutamine synthetase (GS), cyclin D1, Wnt1 inducible signaling pathways protein (WISP1), and matrix metalloproteinase-7(MMP7), P < 0.05. These data suggest that chronic EtOH consumption activates the Wnt/β-catenin signaling pathways to increase hepatocyte proliferation, thus promoting tumorigenesis following an initiating insult to the liver.
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