Figure 6

The miR-26a regulates glucose metabolism in HCT116 cells. (A) Overexpression of miR-26a, by transfection of pENTR-miR-26a in HCT116 cells, elevated glucose uptake. The empty vector pENTR-MIRNA was used as the control. (B) The suppressed expression of miR-26a with its inhibitor treatment greatly induced the decrease of glucose uptake. A non-targeting oligonucleotide was used as the control. The miR-26a inhibits the conversion of pyruvate to acetyl-CoA in HCT116 cells. (C, D) The pyruvate content was increased when HCT116 cells transfected with miR-26a-expressing plasmid pENTR-miR-26a, while the acetly-CoA production was decreased. The empty vector pENTR-MIRNA was used as the control. (E, F) The suppressed expression of miR-26a with its inhibitor treatment induced the decrease of pyruvate content and the up-regulation of the acetly-CoA production. A non-targeting oligonucleotide was used as the control. The average values ± the standard error of the mean (SEM) of three separate experiments were plotted. *p < 0.05, ** p < 0.005.