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- W2885242248 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." @default.
- W2885242248 created "2018-08-22" @default.
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- W2885242248 date "2018-09-11" @default.
- W2885242248 modified "2023-10-16" @default.
- W2885242248 title "Arachidonic acid suppresses hepatic cell growth through <scp>ROS</scp> ‐mediated activation of transglutaminase" @default.
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- W2885242248 doi "https://doi.org/10.1002/2211-5463.12511" @default.
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