Skip to main content
. 2014 Jul 10;111(6):1188–1200. doi: 10.1038/bjc.2014.382

Figure 1.

Figure 1

miR-646 targets the 3′-UTR of NOB1 in luciferase reporter assay. (A) Ideograph of NOB1 mRNA. The predicted miR-646-binding site in the NOB1 3′-UTR. The sequence of wild-type (WT) and mutant (MUT) miR-646 target sites in the NOB1 3′-UTR shown in frame. A point mutation (underlined) was made in the seed region to block the binding between miR-646 and mRNA. (B) The luciferase reporter assay was used to confirm the contribution of the four miR-646 target sites. ACHN cells were co-transfected with luciferase reporter plasmids containing either WT or MUT miR-646 target sites and miR-646, control precursors, LNA-anti-miR NC and LNA-anti-miR-646. miR-646 and full-length wild-type NOB1 3′-UTR decreased luciferase activity. All results were derived from independent experiments performed in triplicate (*P<0.01).