Fig. 4

FOXC1 is a direct target of miR-138. a. A549 cells were treated with RvD1 and the expression level of FOXC1 was analyzed by Western blot, using GAPDH as an endogenous control. **P < 0.01 compared to 0 μg/L RvD1 group. b. A549 cells were transfected with Con, miR-138-5p mimics, Negcon, or miR-138 inhibitor. FOXC1 expression was analyzed by Western blot. **P < 0.01 compared to Con group; ^##P < 0.01compared to NegCon group. c. Putative seed-matching sites (in bold) or mutant sites (red) between miR-138-5p and the 3′-UTR of FOXC1 were analyzed by TargetScan. d. The wild type (WT1 and WT2) and mutant (mut1 and mut2) binding site sequences of miR-138-5p in the 3′ UTR of FOXC1 were cloned into luciferase reporter vectors. A549 cells were co-transfected with the reporter vectors, renilla luciferase vector, and miR-138-5p mimics or Con mimics. After 24 h, the relative luciferase activities were analyzed and data were normalized as the ratio of the Con mimics + WT group. Data are presented as the mean ± SEM from three independent experiments. **P < 0.01 compared to corresponding group