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. 2017 Aug 12;8(43):74582–74594. doi: 10.18632/oncotarget.20216

Figure 4. miR-149 directly inhibited Akt expression.

Figure 4

(A) Predicted miR-149 target sequence of the Akt 3’ -UTR used bioinformatics analysis. (B) Luciferase reporter assay. We co-transfected 50 ng of psiCHECK-2-Akt1 3’ -UTR plasmid and 20 μM of miRNA-149 inhibitor or miRNA-149 inhibitor N.C into HT-29 cells. The N.C treatment group inhibited the luciferase activity of the Akt1 3’-UTR construct. By contrast, miRNA-149 inhibitor increased miR-N.C-inhibited luciferase activity of the Akt1 3’-UTR construct (* p<0.05, ** p<0.01). Each bar represents the mean ± SEM of three independent experiments. (C) Western blot analysis of total Akt, p-Akt and NF-κB-p65 levels in BPIS treated with LPS and miR-149 inhibitors. Data were presented as mean ± SEM (n=3, *p<0.05 vs. control, ## p<0.01 vs. LPS, ×p<0.05). (D) The effect of pretreatment with miRNA-149 inhibitor for 24 h on the BPIS-treated the expression of IL-1β, IL-6 and IL-10 in LPS-stimulated HT-29 cell. Data were expressed as mean ± SEM (n = 4, * p < 0.05).