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. 2018 Mar 1;123(1):19–27. doi: 10.1080/03009734.2018.1440037

Figure 4.

Figure 4.

(A) Luciferase reporter gene assay. The results show that AML1/ETO could activate expression of vector containing the wild-type P1, the P1 mutant, and the wild-type P2, which could not activate the P2 mutant of the 5’-UTR sequence of pre-miR-130a. (NC = negative control luciferase reporter plasmid; P1-WT, P2-WT = luciferase plasmid containing the wild-type P1 or P2 sequence; P1-Mut, P2-Mut = luciferase plasmid containing the mutated P1 or P2 sequence; black = mutated regions). (B) Schematic structure of the luciferase plasmid construct. The results represent the average of three independent evaluations. (C) Growth inhibition by etoposide (5 μM) of transfected SKNO-1 cells after 24 h treatment. The results reveal that growth of SKNO-1 cells was obviously inhibited by etoposide compared to that transfected with the negative control miRNA inhibitor. (D) Caspase 3/7 activity in transfected SKNO-1 cells treated with different concentrations (5 μM and 10 μM) of etoposide for 24 h. The results show that the activity of caspase 3/7 increased significantly in SKNO-1 cells transfected with the miR-130a inhibitor compared to that transfected with the negative control inhibitor (*P = 0.032 and *P = 0.011, respectively).