Fig. 6.

D5P sensitizes cancer cells to GLUT inhibitor by suppressing YAP. A RT‒qPCR of JNK downstream genes (JUN and GADD45A) in HCT116 cells treated under normal conditions, GD or GD supplemented with D5P. B Immunoblotting analysis of phosphorylated YAP (serine 127) and phosphorylated JNK in HCT116 NC and shPGM2 cells treated under normal conditions, GD (4 h) or GD supplemented with D5P or G (4 h). C Schematic diagram of signaling pathways stimulated by GD or GLUT inhibitor treatment. D Immunoblotting analysis of PARP, cleaved PARP (c-PARP) and phosphorylated JNK in HCT116 cells treated under normal conditions or GD with or without D5P supplementation (12 h). Actin was used as a loading control. E Immunoblotting analysis of cleaved PARP (c-PARP), phosphorylated YAP (serine 127), and phosphorylated JNK in HCT116 cells treated with GLUT inhibitor (KL-11743) supplemented with or without D5P (24 h). Actin was used as a loading control. F, G Representative images (F) and quantitative results (G) of soft agar colony formation assays in HCT116 cells treated with KL-11743 supplemented with or without D5P (48 h). H Cell growth curves of HCT116 cells treated with KL-11743, D5P, or both. I, J Representative images (I) and quantitative results (J) of organoid cultures treated with KL-11743 supplemented with or without D5P (60 h). K Immunoblotting analysis of PARP, cleaved PARP (c-PARP) and PNP in HCT116 NC and shPNP cells treated under normal conditions, GD or GD supplemented with D5P (8 h). Actin was used as a loading control. In (A), (G), (H), data are the mean ± S.D.; P values were calculated using Dunnett’s multiple comparison test or Student’s t-test. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns, no significance