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. Author manuscript; available in PMC: 2021 Jun 4.
Published in final edited form as: Oncogene. 2012 Jul 2;32(20):2576–2585. doi: 10.1038/onc.2012.266

Figure 5.

Figure 5.

Several miR-143/145 targets are components in Kras signaling pathways. (ac) Western blot analysis of indicated protein expression (a, c) and qRT–PCR analysis of pri-miR-143/145 expression (b) in HCT116 cells treated with control mimic, miR-143 or miR-145 mimic, or untransfected. (d, e) Luciferase activity derived from the indicated 3′UTR reporter constructs following transfection into MiaPaCa2 cells with control mimic (−) or miR-143 mimics (d, +) or miR-145 mimics (e, +). All values were normalized to renilla luciferase activity produced from a co-transfected control plasmid. For each transfection condition, activity produced from the wild-type construct was normalized to the activity produced by the mutant construct. Error bars represent standard deviations from three independent transfections, each measured in triplicate. P-values for significant experiments indicated (two-tailed t-test) *Double miR-145 mutant. Colored bars represent statistically significantly results. (f, g) Western blot confirmation of miR-143 and miR-145 targets (f) or total JNK (t-JNK) or phospho-JNK (p-JNK) expression (g) in HCT116 cells treated with control mimic, miR-143 or miR-145 mimic or untransfected.