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. 2015 Apr 1;29(7):732–745. doi: 10.1101/gad.257394.114

Figure 1.

Figure 1.

miR-182 negatively regulates Bcl2L12 expression in GBM. (A) Schematic representation of the 3′ UTR of the Bcl2L12 gene, including the miR-182 target site identified by TargetScan. (B) Position of the miR-182-binding site within the 3′ UTR of Bcl2L12 and alignment of miR-182-binding sites among different species. (C) Ranking of miRNAs that bind to the Bcl2L12 3′ UTR sequence. (D) Luciferase activity measured in 293T cells 24 h after transfection of wild-type or mutant Bcl2L12-3′ UTR-pGL3 reporter vectors in combination with synthetic, premature miR-182 or Co-miR sequences at a concentration of 200 nM. (E) Luciferase activity measured 24 h after transfection of 293T cells transiently expressing a Bcl2L12-3′ UTR-pGL3 construct in combination with 200 nM miR-96, miR-182, or miR-183. (F,G) U87MG, LNZ308, and SF767 cells were transfected with 15 nM Co-miR or miR-182 and 100 nM Co-anti-miR or anti-miR-182 for 48 h, and the effects on Bcl2L12 protein and mRNA levels were assessed by Western blotting (F) and RT-qPCR (G). Results are presented as log2 expression. In all cases, Hsp70 is shown as a loading control. Histograms depict mean values ± standard deviations.