Fig. 6: Depletion of STBD1 promotes glycolysis in colorectal cancer cells.

a The number of metabolites identified in each sample by targeted metabolomic profiling. Three biological replicates were performed. b Heatmap showing metabolites in several major pathways detected by targeted metabolomic profiling, from shSTBD1 and shControl HCT116 cells, respectively. For each metabolite, its levels in the six samples were normalized using the z-score method. c–f shControl and shSTBD1 HCT116 cells were cultured with ¹³C₆-glucose-containing medium for 12 h, and then cells were harvested for analysis by LC–MS/MS. 3-PG 3-phosphoglycerate, 2-PG 2-phosphoglycerate, PEP phosphoenolpyruvate, α-KG α-Ketoglutarate. g Mapping metabolites and genes whose abundance changed significantly in shSTBD1 HCT116 cells vs. shControl HCT116 cells to a pathway map. Metabolites and genes (p < 0.05) were shown. Filled circles, ¹³C-labeled carbon atoms; open circles, unlabeled carbon atoms; blue, downregulated; red, upregulated. h shControl and shSTBD1 HCT116 cells were cultured for 48 h, and then the medium was collected to determine the concentration of glucose and lactate concentrations. The lactate or glucose concentration was normalized to the total protein concentration, and the relative concentration was further normalized to that of the shControl HCT116 cells. i shControl and shSTBD1 HCT116 cells were cultured in a low glucose medium for 72 h. The cell viability was then assessed using the MTT assay and normalized to that of cells grown in a high glucose medium. j shControl and shSTBD1 HCT116 cells were incubated in indicated concentrations of 2-DG for 48 h. The cell survival rate in each group was evaluated by the MTT assay, and normalized to that of the control group (0 mM). Experiments h–j were performed in triplicate. Statistical data are presented as mean \(\pm \) SD. Statistical comparisons were performed using an unpaired t test. ***p < 0.001, **p < 0.01, *p < 0.05, ns (not significant), p > 0.05.