ArticleGene expression2019
PRMT1-Dependent Macrophage IL-6 Production Is Required for Alcohol-Induced HCC Progression.
Article in Gene expression, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
35 citing papers in PubMed.
- Protein Posttranslational Modifications in Immunity: Molecular Mechanisms and Therapeutic Targets.MedComm · 2026Review
- Hepatitis B virus, alcohol, and liver cancer.Frontiers in oncology · 2026Review
- PRMT1 in Health and Disease: Emerging Perspectives From Molecular Mechanisms to Therapeutic Strategies.MedComm · 2025Review
- Navigating liver cancer with mouse models: a comprehensive overview of HCC experimental systems.Journal of liver cancer · 2025Article
- Review
- The epigenetic hallmarks of immune cells in cancer.Molecular cancer · 2025Review
- Histone modifications and metabolic reprogramming in tumor-associated macrophages: a potential target of tumor immunotherapy.Frontiers in immunology · 2025Review
- Arginine methylation modification in the malignant progression of benign and malignant liver diseases.iLIVER · 2024Review
- CD58 defines regulatory macrophages within the tumor microenvironment.Communications biology · 2024Article
- Biological impact and therapeutic implication of tumor-associated macrophages in hepatocellular carcinoma.Cell death & disease · 2024Review
- Protective role of 17β-estradiol in alcohol-associated liver fibrosis is mediated by suppression of integrin signaling.Hepatology communications · 2024Article
- EGR3 reduces podocyte inflammatory damage in obesity related glomerulopathy by inhibiting the PRMT1Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Article
- Alcohol-Associated Liver Disease Outcomes: Critical Mechanisms of Liver Injury Progression.Biomolecules · 2024Review
- PRMT1 in human neoplasm: cancer biology and potential therapeutic target.Cell communication and signaling : CCS · 2024Review
- PRMT1 Integrates Immune Microenvironment and Fatty Acid Metabolism Response in Progression of Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2024Article
- Experimental In Vivo Toxicity Models for Alcohol Toxicity.The Eurasian journal of medicine · 2023Article
- Mechanisms of tumor-associated macrophages affecting the progression of hepatocellular carcinoma.Frontiers in pharmacology · 2023Review
- Advancements in the Alcohol-Associated Liver Disease Model.Biomolecules · 2022Review
- Epigenetic Modifications in Tumor-Associated Macrophages: A New Perspective for an Old Foe.Frontiers in immunology · 2022Review
- The role of histone methylase and demethylase in antitumor immunity: A new direction for immunotherapy.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Alcohol is a well-established risk factor for hepatocellular carcinoma, but the mechanisms are not well understood. Several studies suggested that alcohol promotes tumor growth by altering immune cell phenotypes in the liver. Arginine methylation is a common posttranslational modification generated mostly by a single protein, PRMT1. In myeloid cells PRMT1 is a key regulator of immune response. Myeloid-specific PRMT1 knockout mice are hyperresponsive to LPS and deficient in PPARγ-dependent macrophage M2 polarization. We aimed to define the role of myeloid PRMT1 in alcohol-associated liver tumor progression using a mouse model of DEN injection followed by Lieber-DeCarli alcohol liquid diet feeding. We found that PRMT1 knockout mice showed significantly lower expression of IL-10 and IL-6 cytokines in the liver and downstream STAT3 activation, which correlated with reduced number of surface tumors, reduced proliferation, and reduced number of M2 macrophages in the liver as well as within proliferating nodules. We found that blocking IL-6 signaling in alcohol-fed mice reduced the number of tumors and liver proliferation in wild-type mice but not in knockout mice suggesting that reduced IL-6 in PRMT1 knockout mice contributes to the protection from alcohol. Additionally, PRMT1 knockout did not show any protection in tumor formation in the absence of alcohol. Finally, we confirmed that this mechanism is relevant in humans. We found that PRMT1 expression in tumor-associated macrophages correlated with STAT3 activation in human HCC specimens. Taken together, these data suggest that the PRMT1-IL-6-STAT3 axis is an important mechanism of alcohol-associated tumor progression.
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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.