FIGURE 7.

Loss of G0/G1 switch gene 2 (G0S2) expression in chronic myeloid leukaemia (CML) promotes the accumulation of very long‐chain unsaturated fatty acids and altered glycerophospholipid metabolism. (A) Bar graphs show Gene Ontology (GO) analysis for the pathways that are upregulated upon G0S2 ectopic expression (left) or downregulated upon G0S2 knockdown (right) in K562^S cells by RNA sequencing. ^* p < .05. Consistent pathways are indicated in red. (B and C) K562 cells expressing either the non‐targeting control vector (shNT), shRNA targeting G0S2 (shG0S2), or ectopic G0S2 were analysed by untargeted liquid chromatography (LC)/mass spectrometry (MS)‐based lipidomics. shG0S2 resulted in a reduction of very long‐chain di‐ and triglycerides (B). Ectopic G0S2 promoted the accumulation of triglycerides as well as several cell membrane components, including phosphatidylcholine (PC) and phosphatidylethanolamine (PE) species (C). (D) Lipid pathway enrichment was performed based on KEGG databases comparing K562^S cells with G0S2 ectopic expression or knockdown. DAG, diacylglycerol; LPC, lysophosphatidylcholine; LPG, lysophosphatidylglycerol; MAG, monoacylglycerol; PG, phosphatidylglycerol; PI, phosphatidylinositol; PS, phosphatidylserine; TAG, triacylglycerol