FIGURE 8.

Proposed model for G0/G1 switch gene 2 (G0S2) tumour suppressor activity in chronic myeloid leukaemia (CML). The schematic shows the effect of G0S2 on triaclyglyceride (TAG) accumulation both indirectly through adipose triglyceride lipase (ATGL) inhibition, and directly through lysophosphatidic acid acyltransferase (LPAAT) activity. As ectopic G0S2 resulted in the accumulation of diacylglycerides (DAGs), TAGs, and species of phosphatidylcholine (PC) and phosphatidylethanolamine (PE) (Figure 7), our data suggest that G0S2 contributes to lipid homeostasis either by increasing TAG stores or by inducing membrane lipid remodelling. Pathway enrichment analysis of our K562 lipidomics data demonstrated that the lipid pathways affected most by differential G0S2 expression included glycerophospholipid metabolism, autophagy, glycosylphosphatidylinositol (GPI)‐anchor biosynthesis, ferroptosis and choline metabolism in cancer (Figure S9A,B). However, more work needs to be done to determine where these lipid species are being incorporated.