Fig. 8

miR-378c alleviated liver fibrosis by targeting SKP2. A The potential targets of miR-378c were predicted by bioinformatic analyses. B, C The regulatory effects of miR-378c on SKP2 were validated in HEK-293 T and LX-2 cells. D The expression of SKP2, ACAT2, and miR-378c in LX-2 cells with TGF-β1 treatment at different doses and exposure time was detected by RT-qPCR. E The expression of SKP2, α-SMA, and E-cadherin in LX-2 cells with different treatments were detected by western blotting. F, G The expression of SKP2, α-SMA, and E-cadherin were detected by western blotting following different treatments. H The differences of E-cadherin protein degradation induced by CHX were detected in the various groups. I The differences in E-cadherin ubiquitination were detected in the groups with the treatments above. J The morphology of HSCs with TGF-β1, miR-378c mimics, and SKP2 overexpression. K The expression of fibrotic markers in HSCs at different groups was detected by immunofluorescence. L, M Transwell and CCK8 assays were performed to detect the migration and proliferation of HSCs in each group, respectively. N The SKP2, α-SMA, and E-cadherin expression in 5 human fibrotic tissues was detected by immunohistochemical staining. TGF-β1, transformation growth factor- beta; α-SMA, α-smooth muscle actin. **P < 0.01