Pla2g4f, a member of the phospholipase A2 superfamily, catalyzes the hydrolysis of membrane phospholipids, producing free fatty acids and lysophospholipids, thus initiating the arachidonic acid cascade. It is involved in multiple biological processes related to lipid metabolism and has been linked to pathways like glycerophospholipid metabolism [2,4]. Genetic models, such as KO/CKO mouse models, can be valuable for studying its function in vivo.

In triple-negative breast cancer (TNBC), Pla2g4f, specifically expressed in malignant cells, acts as a cell-autonomous metabolic reprogramming factor. It promotes TNBC cell proliferation, migration, and survival in vitro, driven by dysregulated glucose and lipid metabolism, at least in part, through the activation of the AKT/PI3K signaling pathway, highlighting it as a potential therapeutic target [1]. In mice deficient in glutathione peroxidases 1 and 2, Pla2g4f was identified as one of the most likely colitis gene candidates, as GPX metabolizes its products [3].

In conclusion, Pla2g4f plays essential roles in lipid-related metabolic processes. Its study using KO/CKO mouse models has revealed its significance in diseases like TNBC and colitis, providing insights into disease mechanisms and potential therapeutic strategies.