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Fig. 3 | Molecular Cancer

Fig. 3

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

Fig. 3

Requirement of the c-Myc binding site for the butyrate’s inhibitory effects on C13orf25 promoter activity. a Schematic of pGL3 luciferase reporter constructs containing the 1.5-kb promoter region upstream to the miR-17-92a cluster gene in C13orf25, which includes a wildtype functional c-Myc binding site (CATGTG, WT). The pGL3 vectors containing a mutated site (CGATTG, Mut) or a partially deleted site (− − − GTG, Del) were generated as controls. b Promoter activities of the three luciferase reporter constructs in response to butyrate treatment. Two hours after butyrate treatment (2 mM), HCT116 human colon cancer cells were transiently co-transfected with firefly luciferase pGL3 and pRL-TK Renilla luciferase vectors. Twelve h after transfection cells were harvested for measurement of luminescence. Cells without butyrate treatment (Untreated) were analyzed as control. Relative luciferase activity was normalized to the wild-type construct (Untreated). Bars represent means ± SEM. *P < 0.05, n = 4

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