GLS2 Shapes Ferroptosis in Hepatocellular Carcinoma
News, Oncotarget
October 19, 2023“[…] we hope that our findings will inform future decisions regarding treatment of liver disease.”
BUFFALO, NY- October 19, 2023 – A new editorial paper was published in Oncotarget’s Volume 14 on October 19, 2023, entitled, “GLS2 shapes ferroptosis in hepatocellular carcinoma.”
In their new editorial, researchers Sawako Suzuki, Divya Venkatesh, Tomoaki Tanaka, and Carol Prives from Columbia University discuss ferroptosis regulation of GLS2 as a potential therapeutic strategy against liver diseases.
“More than a decade has passed since our group (1) as well as Hu et al., (2) identified glutaminase (GLS2) as a p53 target gene that promotes the tricarboxylic acid cycle (TCA) via α-ketoglutarate (αKG) and lowers oxidative stress via increasing glutathione (GSH) [1, 2].”
Two years after this Dixon et al., [3] described a form of cell death they named ferroptosis which is caused by iron-mediated lipid peroxidation. Then, three years later, Gao et al., reported that GLS2 but not GLS1 is an inducer of ferroptosis in human cancer cells [4]. Ferroptosis had first been shown to be regulated by p53 via repression of SLC7A11 [5]. The circle was closed by a study from the Murphy group who reported that a cancer-related nonsynonymous mutation in p53 (P47S) is correlated with failure to either activate GLS2 expression or produce ferroptosis [6].
“Our recent study (Suzuki et al.) [7] has validated the ability of GLS2 to promote ferroptosis in murine models.”
Continue reading the full paper: DOI: https://doi.org/10.18632/oncotarget.28526
Correspondence to: Carol Prives
Email: clp3@columbia.edu
Keywords: ferroptosis, hepatocellular carcinoma, GLS2, p53, tumor suppression
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