FIGURE 6.

AKR1B10P1 promotes EMT through stabilizing SOX4 mRNA via directly binding with miR‐138 A, RT‐qPCR assay demonstrated that ectopic SOX4 in Hep3B has no significant effect on the expression of AKR1B10, which supports AKR1B10P1 as an up‐streaming regulator of SOX4 (P ＞ 0.05). B, The Western blot analysis illustrated that re‐introducing SOX4 ectopically significant rescued the EMT indicator changes induced by AKR1B10P1 depletion. The E‐cadherin protein was decreased, along with the re‐up‐regulation of N‐cadherin and vimentin (*P < .01). C, Predicted binding sequence of AKR1B10P1 transcript with the seed sequence of miR‐138. The minimum free energy (Mfe) hybridization is calculated as follows: −19.4 kal/mol. D, The direct interaction between AKR1B10P1 and miR‐138 was checked by dual‐luciferase reporter assay. Hep3B cells were transfected with the predicted binding site either wild‐type (WT‐binding site) or mutated (MUT‐binding site). MiR‐138 was up‐regulated in these Hep3B cells (Hep3B/miR‐138) through mimics. Up‐regulation of miR‐138 significantly reduced the luciferase signal of the Hep3B cells of WT‐binding site, compared with the negative control (Hep3B/NigmiR); and also, Hep3B cells of WT‐binding site abolished this suppressive effect (**P ＜ 0.01)