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. 2015 Jul 7;12(4):4917–4924. doi: 10.3892/mmr.2015.4051

Figure 7.

Figure 7

BTG2 is a direct target gene of miR-21. (A) Protein expression levels of BTG2 were increased in HepG2 liver cancer cells transfected with the miR-21 inhibitor, compared with those transfected with the miR-21 inhibitor NC. The protein expression levels of BTG2 decreased in the HepG2 cells transfected with miR-21 mimics, compared with those transfected with the NC. (B) Position of the 3′UTR of BTG2 binding with miR-21. (C) Luciferase activity was significantly decreased in the HepG2 cells following co-ntransfection with the pYr-MirTarget-BTG2-3′U plasmid and miR-21 mimics, but was increased following co-transfection with the pYr-MirTarget-BTG2-3′U plasmid and miR-21 inhibitor, compared with the NC group. (D) Following deletion of the predicted binding site of BTG2 3′UTR, the HepG2 cells were co-transfected with miR-21 mimics and a pYr-MirTarget plasmid (vector), pYr-MirTarget-BTG2-3U plasmid (wild type) or pYr-MirTarget-BTG2-3U-Delete site plasmid (mutation). The results revealed that the luciferase activities were significantly enhanced following deletion of the predicted binding site, compared with the wild-type (mimic) group. *P<0.05, **P<0.01, the mimics NC group compared with miR-21 mimics, and the inhibitor group compared with miR-21 inhibitor group. BTG2, B-cell translocation gene 2; miR-21, microRNA-21; NC, negative control; UTR, untranslated region.