Research Paper Volume 11, Issue 21 pp 9442—9460

Figure 6. DNM3OS competes for miR-361 binding to counteract miR-361-mediated TGFβ1 suppression (A) PrSCs were transfected with si-DNM3OS and examined for the expression of miR-361 by real-time PCR. (B) miR-361 overexpression or inhibition conducted in PrSCs by transfection of miR-361 mimics or inhibitor, as confirmed by real-time PCR. (C) PrSCs were transfected with miR-361 mimics or inhibitor and examined for the expression of DNM3OS by real-time PCR. (D) PrSCs were transfected with miR-361 mimics or inhibitor and examined for the protein levels of TGFβ1. (E) A schematic diagram showing the predicted binding sites between miR-361 and DNM3OS or TGFβ1. Wild- and mutant-type DNM3OS or TGFβ1 3'UTR luciferase reporter vectors were constructed. Mutant-type vectors contained a 7- or 10- bp mutation in the predicted miR-361 binding site. (F–G) 293T cells were cotransfected with the vectors and miR-361 mimics or inhibitors and examined for luciferase activity. **P<0.01.