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. 2016 Feb 1;6:20314. doi: 10.1038/srep20314

Figure 6. MiR-155 regulated Wnt/β-catenin and Akt signaling in primary fibroblast by targeting CK1α and SHIP-1 with TGF-β stimulation.

Figure 6

(a) Depiction of mouse CK1α (csnk1a1) and SHIP-1 (inpp5d) mRNA 3′ UTR sequence alignment with miR-155 sequence. Mutant sites are marked green. (b) MiR-155 bound directly to the 3′ UTR of mouse CK1α mRNA. A luciferase reporter assay was co-transfected with miR-155 mimic or normal control (n.c.) into HEK293 cells. ***P < 0.001, ANOVA. (c) Similarly, miR-155 bound directly to the 3′ UTR of mouse SHIP-1 mRNA. ***P < 0.001, ANOVA. (d) MiR-155 inhibitor up-regulated CK1α and degradation of β-catenin spontaneously. The numbers below lanes represent optic density ration to GAPDH. (e) Similarly, miR-155 regulated protein levels of SHIP-1 and phosphorylation of Akt. The numbers below lanes represent optic density ration to GAPDH.