ArticleFEBS open bio2018
Arachidonic acid suppresses hepatic cell growth through ROS-mediated activation of transglutaminase.
Article in FEBS open bio, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Metabolites involvement in the growth and spread of liver cancer.Liver research (Beijing, China) · 2025Review
- Transglutaminase 2 Stimulates Cell Proliferation and Modulates Transforming Growth Factor-Beta Signaling Pathway Independently of Epithelial-Mesenchymal Transition in Hepatocellular Carcinoma Cells.International journal of molecular sciences · 2025Article
- A high-throughput screening platform to identifyFrontiers in oncology · 2025Article
- Targeting transglutaminase 2 mediated exostosin glycosyltransferase 1 signaling in liver cancer stem cells with acyclic retinoid.Cell death & disease · 2023Article
- Biliary Metabolome Profiling for Evaluation of Liver Metabolism and Biliary Tract Function Related to Organ Preservation Method and Degree of Ischemia in a Porcine Model.International journal of molecular sciences · 2023Article
- Metabolomics reveals potential plateau adaptability by regulating inflammatory response and oxidative stress-related metabolism and energy metabolism pathways in yak.Journal of animal science and technology · 2022Article
- Transglutaminase 2 as a Marker for Inflammation and Therapeutic Target in Sepsis.International journal of molecular sciences · 2021Review
- Synthesis and Anti-Hepatocarcinoma Effect of Amino Acid Derivatives of Pyxinol and Ocotillol.Molecules (Basel, Switzerland) · 2021Article
- Prevention of arachidonic acid-induced liver injury by controlling oxidative stress-mediated transglutaminase activation with garlic extracts.Experimental and therapeutic medicine · 2020Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously reported a profound augmentation in the hepatic levels of a pro-inflammatory precursor, arachidonic acid (AA), during liver tumorigenesis. Here, we report a critical role of the induced reactive oxygen species (ROS)-mediated cellular activation of a protein cross-linking enzyme, transglutaminase 2 (TG2), in liver injury by AA. In cultures of hepatic cells, AA dose-dependently suppressed cell growth, which accompanied the induced nuclear accumulation of TG2, as demonstrated in EGFP-tagged, TG2-overexpressing hepatic cells. A chemical inhibitor/shRNA that acts against TG2 prevented AA-mediated cell growth suppression. In addition, AA provoked significant production of ROS, and antioxidants blocked AA-induced activation of nuclear TG2 and hepatic cell growth suppression. We propose that AA-mediated oxidative stress and TG2 transamidase activity might contribute to chronic liver injury and inflammation and thereby serve as potential therapeutic targets for the chemoprevention of hepatocellular carcinoma.
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Registered trials
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