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. 2020 Sep 15;12(9):5465–5480.

Figure 5.

Figure 5

AKR1B10P1 transcript sponges miR-138 to exert stabilization effect on SOX4 expression. A. Predicted binding site of AKR1B10P1 transcript potentially interacts with the seed sequence of miR-138. The minimum free energy (Mfe) hybridization is calculated as: -19.4 kal/mol. B. RT-qPCR was conducted for measuring the expression of miR-138. As the scatter plot demonstrated, expression of miR-138 was negatively related with AKR1B10P1 transcript (Spearman R=0.4351, P < 0.0001). C. The direct interaction between AKR1B10P1 and miR-138 was validated by applying Dual-luciferase reporter assay. Hep3B cells were transfected with the predicted binding site either wildtype (AKR1B10P1/pMIR/WT) or mutated (AKR1B10P1/pMIR/MUT). Up-regulation of miR-138 significantly reduced the luciferase signal of the Hep3B cells of AKR1B10P1/pMIR/WT, compared with the negative control (Hep3B/NigmiR); And also, Hep3B cells of AKR1B10P1/pMIR/MUT site abolished this suppressive effect (**P < 0.01).