Fig. 2
From: m6A-dependent glycolysis enhances colorectal cancer progression
METTL3 drives glycolytic metabolism in CRC. (a-b) Lactate production (a), glucose uptake (b) were measured in HCT116 WT and METTL3-KO cells by colorimetric analysis, n = 3, nonparametric Mann–Whitney test. (c-d) Lactate production (c) and glucose uptake (d) were measured in HCT116 CRC cells transfected with control siRNA and METTL3 siRNA1/2 by colorimetric analysis; n = 3, nonparametric Mann–Whitney test. (e-f) ECAR was detected in HCT116 WT, METTL3- knockout cells (e) and HCT116 CRC cells transfected with control siRNA or METTL3 siRNA1/2 (f), n = 4, nonparametric Mann–Whitney test. (g-i) Lactate production (g), glucose uptake (h) and ECAR (i) were assessed in DLD1 cells transfected with pcDNA3.1, pcDNA3.1-METTL3 and pcDNA3.1-METTL3-mut, n = 3, nonparametric Mann–Whitney test. (j) Representative images of 18F-FDG uptake by micro-PET imaging in WT and METTL3-KO xenograft mouse models. White circles indicated tumor glucose uptake. Maximum uptake values (SUVmax) for xenografts measured by FDG-PET were presented, nonparametric Mann–Whitney test. (k) Representative images of 18F-FDG uptake by micro-PET imaging in control virus, overexpression of METTL3 or METTL3-mut virus xenograft mouse models. White circles indicated tumor glucose uptake. Maximum uptake values (SUVmax) for xenografts measured by FDG-PET were presented, nonparametric Mann–Whitney test. Fig. 2k and Fig. 6k shared experimental controls and METTL3-overexpression group. (WT, wild type; METTL3-KO, METTL3-knockout; n = 3)