Skip to main content
. 2019 Dec 1;9(12):2665–2678.

Figure 6.

Figure 6

p53-miR-3196-FOXP4 axis plays a key role in HCC suppression. A, B. miR-3196 together with 3’ UTR of FOXP4 was transfected into HepG2 cells with or without p53 knockdown. The protein levels of FOXP4 and the luciferase activity were measured. Data represent the mean ± SD of three independent experiments. **P<0.01 vs. control. C, D. miR-3196 inhibitor together with 3’ UTR of FOXP4 was transfected into BEL7402 cells with or without p53 overexpression. The protein levels of FOXP4 and the luciferase activity were measured. Data represent the mean ± SD of three independent experiments. **P<0.01 vs. control. E, F. p53 was knocked down in HepG2 cells together with miR-3196 overexpression or FOXP4 knockdown. The cell proliferation was examined by a colony formation assay. Data represent the mean ± SD of three independent experiments. ***P<0.001 vs. control. G, H. miR-3196 was overexpressed in HepG2 cells together with p53 knockdown. The cells were then treated with 2 μM Dox for 36 h and cell apoptosis was analyzed by western blotting and Flow Cytometer. I, J. FOXP4 was knocked down in HepG2 cells together with p53 knockdown. The cells were then treated with 2 μM Dox for 36 h and cell apoptosis was analyzed by western blotting and Flow Cytometer. K. miR-3196 inhibitor was transfected into BEL7402 cells with or without p53 overexpression. The cells were then treated with 2 μM Dox for 36 h and cell apoptosis was analyzed by western blotting.