Hepatocyte Necrosis Induced by Oxidative Stress and IL-1α Release Mediate Carcinogen-Induced Compensatory Proliferation and Liver Tumorigenesis
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Hepatocyte I kappaB kinase beta (IKK beta) inhibits hepatocarcinogenesis by suppressing accumulation of reactive oxygen species (ROS) and liver damage, whereas JNK1 activation promotes ROS accumulation, liver damage, and carcinogenesis. We examined whether hepatocyte p38 alpha, found to inhibit liver carcinogenesis, acts similarly to IKK beta in control of ROS metabolism and cell death. Hepatocyte-specific p38 alpha ablation enhanced ROS accumulation and liver damage, which were prevented upon administration of an antioxidant. In addition to elevated ROS accumulation, hepatocyte death, augmented by loss of either IKK beta or p38 alpha, was associated with release of IL-1 alpha. Inhibition of IL-1 alpha action or ablation of its receptor inhibited carcinogen-induced compensatory proliferation and liver tumorigenesis. IL-1 alpha release by necrotic hepatocytes is therefore an important mediator of liver tumorigenesis.
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IL-1α released during hepatocyte necrosis contributes to carcinogen-induced liver tumorigenesis in mice.
“In addition, IL-1α released during hepatocyte necrosis contributes to carcinogen-induced liver tumorigenesis in mice77.”
From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [77]
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- Authors
- Sakurai, T., He, G., Matsuzawa, A., Yu, G.-Y., Maeda, S., Hardiman, G., & Karin, M.
- Affiliations
- Kyoto University (JP)
- University of California San Diego (US)
- The Institute of Medical Science, Asahi Life Foundation (JP)
- Corresponding author
- Karin, Michael
- ORCID
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2008-08
- Volume
- 14
- Issue
- 2
- Pages
- 156-165
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC2707922
- OpenAlex
- W1992481999
- Cited by
- 487
- References
- 55
- Citations by year
- 2026: 4 · 2025: 9 · 2024: 23 · 2023: 24 · 2022: 27 · 2021: 30 · 2020: 26 · 2019: 29 · 2018: 24 · 2017: 26 · 2016: 29 · 2015: 35 · 2014: 27 · 2013: 43 · 2012: 38
- FWCI
- 22.61
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Research Portal (Queen's University Belfast) (submittedVersion)
- Funders
- Takeda Science Foundation
- National Institutes of Health
- Japan Society for the Promotion of Science
- National Cancer Institute (R01CA118165, CA118165)
- National Institute of Diabetes and Digestive and Kidney Diseases (P30DK063491)
- National Institute of Environmental Health Sciences (ES004151, ES0100337, ES-006376, R37ES004151, R01ES006376)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
- Keywords
- liver necrosis, oxidative stress, reactive oxygen species, IL-1α, hepatocarcinogenesis, compensatory proliferation, IKKβ, JNK1, hepatocyte-specific knockout, antioxidants, hepatocyte death, IL-1 receptor
- MeSH terms
- Animals, Antioxidants, Carcinogens, Diethylnitrosamine, Enzyme Activation, Heat-Shock Proteins, Liver Neoplasms, Models, Biological, Necrosis, Neoplasm Proteins, Signal Transduction, Interleukin-6, Cell Death, Reactive Oxygen Species, Oxidative Stress, Molecular Chaperones, Hepatocytes, JNK Mitogen-Activated Protein Kinases, p38 Mitogen-Activated Protein Kinases, Cell Proliferation, Mice, I-kappa B Kinase, Transcription Factor CHOP, Interleukin-1alpha
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