Research Paper Volume 11, Issue 12 pp 4075—4089

TGF-β1 enhances FOXO3 expression in human synovial fibroblasts by inhibiting miR-92a through AMPK and p38 pathways


Figure 5. The binding of miR-92a to FOXO3 3' UTR mitigates TGF-β1-induced increases in FOXO3 expression. (A) Diagram of the miR-92a binding site in the wild-type and mutant FOXO3 3’UTRs. (B, C) OASFs were transfected with the wt-FOXO3-3’UTR (B) or mt-FOXO3-3’UTR (C) plasmid with or without miR-92a mimic, then stimulated with TGF-β1. FOXO3 promoter activity was expressed as the relative luciferase activity. (D) OASFs were pretreated with Ara A, compound C and SB203580 for 30 min, then incubated with TGF-β1 (10 ng/ml) for 24 h. The expression of miR-92a was examined by qPCR. Results are expressed as the mean ± SEM. *p < 0.05 as compared with the control group; #p < 0.05 as compared with the TGF-β1-treated group.