Proteomic alterations in the context of survival signaling and redox homeostasis linked to de novo fatty acid biosynthesis

Cell death programs like apoptosis, necroptosis, and ferroptosis have an oxidative component linked to lipid metabolism that impacts membrane homeostasis. Evidence for cross-talk between these programs is emerging, highlighting the need for overarching regulatory mechanisms. We investigated changes in the proteome of NIH-3T3 fibroblasts upon induction of cytotoxic stress (valinomycin, myrtucommulone A or serum depletion) and SCD1 inhibition (CAY10566) and addressed the potential of oleic acid (18:1), PI(18:1/18:1) and PI(16:0/16:0) to compensate for the decrease in de novo fatty acid biosynthesis. Please note that parts of the data were previously uploaded to project PXD025396 [http://www.ebi.ac.uk/pride/archive/projects/PXD025396] and reanalyzed for the current project (w/o, VAL, MC, CAY, CAY+ PI(18:1/18:1) and CAY + PI(16:0/16:0)).