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. 2020 Apr 3;46(1):141–148. doi: 10.3892/ijmm.2020.4565

Figure 2.

Figure 2

miR-1290 directly targets Napsin A to modulate A549 cell proliferation and TGF-β1-induced fibrosis. (A) Schematic diagram showing the predicted binding site between miR-1290 and Napsin A 3′UTR. Wild- and mutant-type Napsin A 3′UTR luciferase reporter vectors were constructed. The mutant-type Napsin A 3′UTR vector contained a 7-bp mutation in the predicted miR-1290 binding site. These vectors were co-transfected into 293 cells with miR-1290 mimics or inhibitor and the luciferase activity was determined. (B) miR-1290 overexpression and inhibition in A549 cells were achieved by transfection with miR-1290 mimics or an inhibitor, and results were confirmed by RT-qPCR. (C) Napsin A mRNA expression in response to miR-1290 overexpression or inhibition was determined by RT-qPCR. (D) Viability of A549 cells in which miR-1290 was overexpressed or inhibited was determined by MTT assays. (E) Protein levels of Napsin A, α-SMA, Collagen I, AKT and p-AKT in A549 cells in which miR-1290 was overexpressed or inhibited were determined by western blot analysis. *P<0.05 and **P<0.01, compared to the NC (negative control) inhibitor group; ##P<0.01, compared to the NC (negative control) mimics group.