Fig. 5: MiR-1246 and miR-10b-5p promote glioma cell migration and invasion by directly targeting FRK and TFAP2A.

a Schematic representation of the predicted miR-1246 binding site in the 3’UTR of FRK, the mutated miR-1246 binding site in the 3′UTR of FRK, the predicted miR-10b-5p binding site in the 3′UTR of TFAP2A and the mutated miR-10b-5p binding site in the 3′UTR of TFAP2A. b Left: miR-NC or miR-1246 and luciferase vector encoding the wild-type or mutant 3′UTR of FRK were co-transfected into 293T cells and the relative luciferase activity was measured. Right: miR-NC or miR-10b-5p and luciferase vector encoding the wild-type or mutant 3′UTR of TFAP2A were co-transfected into 293T cells and the relative luciferase activity was measured. c Western blot analysis of FRK and TFAP2A in miR-NC-, miR-1246-, and miR-10b-5p-transfected U87MG and U251 glioma cells. d Representative images of indicated treated U87MG and U251 glioma cells that migrated (without Matrigel coating) to the bottom surface. Scale bar, 100 μm. e Quantification of indicated treated U87MG and U251 glioma cells that migrated (without Matrigel coating) to the bottom surface. f, g Western blot analysis of FRK, TFAP2A, N-cadherin, MMP2, MMP9, and vimentin levels in indicated treated U87MG and U251 glioma cells. Data are shown as the mean ± SD of three independent experiments. Statistical significance was determined using Student’s t test and one-way ANOVA test (*P < 0.05; **P < 0.01).