Fig. 2

FXR upregulates miR-122 expression and suppresses the expression of miR-122 target genes. a Hep3B cells were treated with GW4064 (0.5 or 5 μM) or vehicle DMSO for 24 h, and then the expression of pri-miR-122 and mature miR-122 was assayed using qRT-PCR. b and c Hep3B cells were treated with GW4064 (0.5 or 5 μM) or vehicle DMSO for 48 h, and then the expression of miR-122 target genes including IGF-1R and cyclin G1 was separately examined by qRT-PCR (b) and Western blotting (c). d Hep3B cells were transfected with 10 nM control siRNA or FXR siRNA for 24 h, and then the level of FXR protein was detected by Western blotting. e and f After transfection with control siRNA or FXR siRNA for 24 h, Hep3B cells were treated with vehicle DMSO or 5 μM GW4064 for 24 h, and then the expression of miR-122 and its target genes including IGF-1R and cyclin G1 was determined by qRT-PCR (e) and Western blotting (f). g and h After transfection with 50 nM antagomir-122 or antagomir negative control (NC) for 6 h, Hep3B cells were treated with vehicle DMSO or 5 μM GW4064 for 48 h, and then the expression of IGF-1R and cyclin G1 was analyzed by qRT-PCR (G) and Western blotting (h). β-actin was used as a control for the examination of FXR, pri-miR-122, IGF-1R and cyclin G1, while U6 snRNA as a control for the detection of mature miR-122. *P < 0.05, **P < 0.01 vs vehicle