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. 2015 Aug 6;48(5):582–592. doi: 10.1111/cpr.12201

Figure 4.

Figure 4

miR‐34c‐3p directly targeted eIF 4E in NSCLC cells. (a) Sequences of miR‐34c‐3p binding sites within eIF4E 3′UTR in vertebrates. Wild‐type eIF4E 3′UTR was fused into pMIR luciferase reporter plasmid. eIF4E 3′UTR mutant represents the reporter constructs containing mutated nucleotides (red). (b and c) Relative luciferase activities of plasmids carrying wild‐type or mutant eIF4E 3′UTR in A549 and H157 cells co‐transfected with miR‐NC versus miR‐34c‐3p (b) and miR‐in‐NC versus miR‐34c‐3p‐in (c). n = 4. (d and f) RT‐PCR analysis of eIF4E mRNA levels in NSCLC cells transfected with miR‐NC or miR‐34c‐3p (d), miR‐in‐NC or miR‐34c‐3p‐in (f). Expression of eIF4E was normalized to GAPDH. n = 4. (e and g) western blot analysis of eIF4E expression in A549 and H157 cells transfected with miR‐34c‐3p compared to miR‐NC (e) and miR‐34c‐3p‐in compared to miR‐in‐NC (g). GAPDH was used as a loading control. *P < 0.05, **P < 0.01 compared to miR‐NC‐ or miR‐in‐NC‐transfected cells.