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. 2016 Nov 24;8(3):4629–4641. doi: 10.18632/oncotarget.13542

Figure 2. miR-182 is directly suppressed by SNAI1.

Figure 2

A. SNAI1 protein level was detected in MCF-10A cells transfected with SNAI1 or a control vector, using Western Blot (up). Then, the endogenous expression of miR-182 in these two groups was examined using qRT-PCR (down). The values were normalized to U6. B. MCF-10A cells were transfected with SNAI1 siRNA (siSNAI1) or a control siRNA (siNC), then qRT-PCR was performed to detect the efficiency of SNAI1 knockdown (left) and the endogenous expression of miR-182 (right). The values were normalized to GAPDH and U6, respectively. C. Schematic of 6 typical SNAI1-responsive elements (SREs) of miR-182 promoter region using the CONSITE program. D. MCF-10A cells were transfected with SNAI1 or a control vector, then the ChIP assays were performed with antibody against SNAI1 or control IgG. The percentages of input of coprecipitating DNAs were detected by qPCR. Here shows the ChIP assay results for SRE2 of miR-182 promoter physically associated with SNAI1. E. A description of SRE2 of miR-182 promoter (WT) and its mutation (Mut) reporter constructs. F. Luciferase reporter assay of HEK293T cells co-transfected with SNAI1 and luciferase plasmids, that contained the SRE2 of miR-182 promoter in the form of either wild-type (WT) or mutation (Mut). Error bars in A, B, D and F represent mean ± SEM. *P<0.05. **P<0.01.