Fig. 3: SLFN11 knockout promotes G3P accumulation in EWS cells. | Cell Death & Disease

Fig. 3: SLFN11 knockout promotes G3P accumulation in EWS cells.

From: Targeting glycerophospholipid biosynthesis overcomes chemoresistance driven by SLFN11 loss in Ewing sarcoma

Fig. 3: SLFN11 knockout promotes G3P accumulation in EWS cells.

Volcano plots illustrating differentially abundant metabolites between SLFN11−/− and WT cells in (a) ES-8 and (b) SK ES-1 cell lines. Red dots indicate significantly upregulated metabolites involved in GPL biosynthesis. c Schematic overview of U-¹³C glucose tracing using LC-MS to assess ¹³C enrichment in downstream metabolic intermediates across cell lines. Glc and Gln correspond to glucose and glutamine, respectively. d Schematic showing U-¹³C glucose-derived carbon incorporation into glycolysis and GPL biosynthesis. Purple circles represent ¹³C-labeled carbon atoms. e Bar graph showing percentage differences in ¹³C enrichment of the M + 3 isotopologue for DHAP and G3P in WT and SLFN11−/− ES-8, SK ES-1 and EW-8 cell lines following 24 h labeling with U-¹³C glucose. G3P, glycerol-3-phosphate; DHAP, dihydroxyacetone phosphate. Data represent mean ± SD; n = 5. Statistical analysis was performed using a paired two-tailed Student’s t test for each comparison. *** p < 0.001, * p < 0.05. SD standard deviation; n number of replicates.

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