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. 2014 Oct 14;9(10):e110074. doi: 10.1371/journal.pone.0110074

Figure 4. MiR-199a inhibits cell proliferation by directly targeting FZD7.

Figure 4

(A) Dual luciferase assays were performed in HepG2-199a and HepG2-NC cells transfected with the firefly luciferase reporter and the control vectors containing Renilla luciferase. The results showed that miR-199a could significantly suppress the luciferase activity of the reporter containing the 3′UTR of FZD7 but had no significant effect on the reporter containing the mutated binding site of FZD7. The data shown are the means ± SD of three independent experiments. (B) The sequences of the miR-199a binding sites within the 3′UTR of FZD7 and the mutated binding site are presented. (C) qRT-PCR analysis showing that the mRNA of FZD7 was significantly decreased in HepG2-199a cells compared with HepG2-NC cells. (D) Western blot analysis confirming that the expression of FZD7 and of its downstream genes was significantly inhibited by miR-199a. β-actin was used as the internal control. (E) The expression of the FZD7 protein in HepG2 and SMMC-7721 cells was higher compared with that in normal Chang liver cells.