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Fig. 5 | BMC Cancer

Fig. 5

From: MiR-449a suppresses the epithelial-mesenchymal transition and metastasis of hepatocellular carcinoma by multiple targets

Fig. 5

FOS and MET are targets of miR-449a. a Schematic illustration of the predicted miR-449a-binding sites in FOS and MET 3’-UTR. b FOS and MET were targets of miR-449a. MiR report constructs, containing a wildtype and two mutated FOS and MET 3’-UTR, were co-transfected into LM9 cells which were infected by miRcontrol-lentivirus or miR-449a-lentivirus. Relative repression of firefly luciferase expression was standardised to a transfection control. Data of the reporter assays are the means ± SE of three independent experiments. c mRNA levels of FOS and MET after miR-449a-induced expression in LM9 cells examined by real-time PCR. d Ectopic expression of miR-449a decreased endogenous levels of FOS and MET protein in LM9 cells. LM9 cells were infected with either lentivirus-miR-control or lentivirus-miR-449a for 72 h. FOS and MET expression was assessed by western blot. e The antagonism of endogenous miR-449a increased FOS and MET expression in the HepG2 cell. Anti-miR-NC or anti-miR- 449a was transfected into HepG2 cells for 72 h and analyzed by immunoblotting. α-tubulin was used as a loading control

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