Fig. 3: miR-27a controls the destiny of glucose in CRC cells.

a Kinetic profile of extracellular acidification rate (ECAR) in HCT116 and SW480 miR-27a_KD and HT29 miR-27a_OE cells and their relative CTRL_KD and CTRL_OE cells, respectively. ECAR, expressed as mpH/min, was measured in real time, under basal conditions and in response to glucose, oligomycin and 2DG. Data are reported as mean ± SEM of experiments performed in triplicate; the means values were compared by one-way analysis of variance test (ANOVA). Statistical significance was considered when *p ≤ 0.05, **p ≤ 0.01, ***p < 0.001. The histograms show the quantification of ECAR kinetic profile in: (a) basal glycolysis, (b) basal glycolysis post-glucose injection, (c) glycolytic capacity, (d) glycolytic reserve (d = c − b). b “Cell energy phenotype profile”. The drawings illustrate the metabolic potential of the same cells as in a as a measure of cells’ ability to respond to an energy request after a stress via mitochondrial respiration and glycolysis. The baseline phenotype (levels of mitochondrial respiration and glycolysis in basal conditions) is reported on the left of each drawing; the stressed phenotype (relative utilisation of aerobic respiration and glycolysis upon stressed conditions) is on the right. Data are reported as mean ± SEM of experiments performed in triplicate; the means values were compared by one-way analysis of variance test (ANOVA). Statistical significance was considered when ***p < 0.001. c Immunoblot analysis of glycolytic enzymes levels in the same cell lines as in a. β-Tubulin was used for protein loading normalisation. Data are reported as mean ± SEM of experiments performed in triplicate; the means values were compared by one-way analysis of variance test (ANOVA). Statistical significance was considered when *p ≤ 0.05, **p ≤ 0.01, ***p < 0.001.