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Fig. 4 | Molecular Cancer

Fig. 4

From: Butyrate inhibits pro-proliferative miR-92a by diminishing c-Myc-induced miR-17-92a cluster transcription in human colon cancer cells

Fig. 4

Effect of silencing c-Myc expression on miR-92a in HCT116 cells. HCT116 human colon cancer cells were transfected with predesigned MISSION siRNAs, an endoribonuclease-derived pool comprising a heterogeneous mixture of siRNAs targeting c-Myc mRNA (si-cMyc), or control siRNA (si-Cont) using Lipofectamine 2000 for 24 h before cell harvest. Cells treated with Lipofectamine 2000 alone (Lipo) served as control. a Protein levels of c-Myc and β-actin were analyzed by immunoblotting. The image shown is representative of four individual experiments. b Relative c-Myc protein levels were measured by densitometry. In HCT116 cells with control and reduced levels of c-Myc expression, qPCR was used to measure the abundance of c pri-miR-17-92a and d miR-92a. Bars represent means ± SEM. *P < 0.05, n = 4. e Eight hours after si-RNA transfection, HCT-116 cells were transiently co-transfected with pGL3 luciferase vectors containing wild-type (WT) or mutated (Mut) promoter region of miR-17-92a cluster as described in Fig. 3a and pRL-TK Renilla luciferase vectors. Twenty four hours after luciferase vector transfection, cells were harvested for measurement of luminescence. Relative luciferase activity was normalized to the wild-type control (Lipo). Bars represent means ± SEM. *P < 0.05, n = 4

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