Fig. 4

CCHE1 promoted melanoma cell glycolysis. A CCHE1 overexpression promoted the glucose uptake (left panel) and lactate levels (right panel). B CCHE1 depletion significantly reduced both the glucose uptake (left panel) and lactate production (right panel) of melanoma cells compared with the control cells. C, D Melanoma cells were transfected with control vector of CCHE1. The glycolysis fulx was determined by detecting the EACR using the Seahorse analyzer. 10 mM glucose, 1 μM ATP synthase inhibitor oligomycin, and 50 mM 2-DG was added at the indicated time points. The values of glycolysis, glycolytic capacity and glycolytic reserve were calculated by Seahorse XF24 software. Significantly enhanced glycolysis flux was observed with CCHE1 overexpression. E, F CCHE1 knockdown inhibited the glycolysis fulx both in A375 and G-361 cells. In C-F, data was obtained from three independent experiments and statistical analysis was performed via the two-sided Student’s t test. G The tumors of A375 xenograft mouse model were isolated at the end of the experiment and the lactate levels were detected. The lactate levels of tumors carrying CCHE1 depletion ware lower than that of the shRNA-control group. Data was normalized to protein concentrations. * p < 0.05, ** p < 0.01, ***p < 0.001 vs. control