Skip to main content
Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

From: METTL16 promotes glycolytic metabolism reprogramming and colorectal cancer progression

Fig. 5

METTL16/SOGA1 axis enhances glycolysis by targeting PDK4 in CRC cells. A-B SOGA1 knockdown decreased glucose consumption (A) and lactate production (B) in SW620 cells. C-D The ECAR (C) and OCR (D) profile were measured in SOGA1 knockdown SW620 cells with a Seahorse XF24 analyser. The metabolic inhibitors were injected sequentially at different time points as indicated. E-F METTL16 knockdown decreased glucose consumption (E) and lactate production F in SW620 cells. G-H The ECAR (G) and OCR (H) profile were measured in METTL16 knockdown SW620 cells. I-J METTL16 overexpression increased glucose consumption (I) and lactate production (J) in SW620 cells. K-L PDK4 was identified as METTL16/SOGA1 regulated gene. The expression of a panel of glucose metabolism-related genes was detected by qRT-PCR in SOGA1 knockdown (K) or METTL16 overexpression (L) cells and their corresponding control cells. M PDK4 mRNA expression in HCT15 cells with SOGA1 knockdown was detected by qRT-PCR. N PDK4 protein expression in HCT15 and SW620 cells with SOGA1 knockdown was detected by western blotting. O PDK4 protein expression in HCT15 and SW620 cells with METTL16 knockdown was detected by western blotting. **P < 0.01, ***P < 0.001, ****P < 0.0001

Back to article page