Fig. 5

PAK6 is a directly target of miR-3191 in HCC cells (A) A potential target site for miR-3191 in the 3’-UTR of human PAK6 mRNA, as predicted by the program TargetScan. To disrupt the interaction between miR-3191 and PAK6 mRNA, the target site was mutated. (B) Luciferase activity of PAK6‑3’‑UTR‑WT or PAK6‑3’‑UTR‑MUT plasmids in Huh7/Hep3B miR‑3191 mimic and control cells (n = 3). (C) Luciferase activity of PAK6‑3’‑UTR‑WT or PAK6‑3’‑UTR‑MUT plasmids in Huh7/Hep3B miR‑3191 inhibitor and control cells (n = 3). (D) Expression of PAK6 in Huh7 and Hep3B cells treated with miR-3191 mimic and control. (E) Relative PAK6 mRNA expression in Huh7 and Hep3B treated with miR-3191 mimic and control cells (n = 3). (F) Western blot analysis of PAK6 protein expression in Huh7 and Hep3B treated with miR-3191 mimic and control cells. (G) PAK6 mRNA expression in Huh7 and Hep3B treated with miR-3191 inhibitor and control cells (n = 3). (H) PAK6 protein expression in Huh7 and Hep3B treated with miR-3191 inhibitor and control cells. (I) Significant correlation between miR-3191 and PAK6 expression in human HCC tissues (n = 40). (J) Overall survival time after surgery of the patients were compared between the ‘‘PAK6 low’’ (n = 90) and ‘‘PAK6 high’’ (n = 90) groups, p < 0.05. (K) Kaplan–Meier analysis of overall survival of TNBC patients with high or low miR-3191 and PAK6. p < 0.05