Fig. 3

HMGB1 is a direct target of miR-107. a Diagram of the binding site between miR-107 and the HMGB1 3′ UTR. The reporter vectors contain the wild-type (WT) or mutant (Mut) HMGB1 3′ UTR. b Dual-luciferase reporter assay of the HMGB1 3′ UTR. The reporter vectors containing the WT or Mut HMGB1 3′ UTR were transfected into NPCs. Luciferase activity was shown to be significantly downregulated after HBO treatment (**p < 0.01; n = 4) in the constructs harboring the WT but not in the Mut 3′ UTR (p > 0.05, n = 4). c Real-time PCR analysis of HMGB1 mRNA expression in degenerated NPCs transfected with miR-107 inhibitors. HMGB1 mRNA expression was downregulated after HBO treatment (*p < 0.05; n = 4). Anti-miR-107 reversed the suppressive effects of HBO (p > 0.05; n = 4). d Western blot analysis of HMGB1 protein expression in NPCs transfected with miR-107 inhibitors. Values were normalized against β-actin. HMGB1 protein expression was significantly downregulated after HBO treatment (**p < 0.01; n = 4). MiR-107 inhibitors reversed the suppressive effects of HBO (p > 0.05; n = 4). WT wild type, Mut mutant