Fig 1: Targeting of MTA3 by miR-32 has a direct functional effect on liver fibrosis under HG conditions. (A) Sequence alignment highlighting complementary nucleotides between miR-32 and the 3'-UTR of MTA3; letters in red indicate matched bases. (B) Luciferase reporter gene assay exhibiting significantly reduced luciferase activities when using miR-32 mimics, and AMO-32 abolished the repressive effects. The mutated construct did not affect luciferase activity (n=5/group). *P<0.05 vs. control; #P<0.05 vs. miR-32. (C) MTA3 protein and mRNA expression in the livers of control and T2DM rats (n=5/group). *P<0.05 vs. control group. (D) MTA3 protein and mRNA expression in HG-treated AML12 cells (n=5/group). *P<0.05 vs. control group; #P<0.05 vs. LG group. (E) Effect of miR-32 on MTA3 expression in AML12 cells (n=5/group). *P<0.05 vs. control group. (F) MTA3 protein and mRNA expression in AML12 cells following transfection with AMO-32 under hyperglycemic conditions (n=5/group). *P<0.05 vs. HG group. miR-32, miR-32 mimic; T2DM, type 2 diabetes mellitus; AMO-32, antisense inhibitor of miR-32; AMO-NC, negative control for AMO-32; HG, high glucose (6,000 mg/l); 3'-UTR, 3'-untranslated region; MTA3, metastasis-associated protein MTA3.