Fig. 6From: ZNF326 promotes malignant phenotype of glioma by up-regulating HDAC7 expression and activating Wnt pathwayZNF326 down-regulates acetylation of β-catenin at Lys49 and phosphorylation at Ser45 through increasing HDAC7 expression. a-d ZNF326 and siRNA-HDAC7 were co-transfected into U87, or the inhibitor TSA (10 nM) was added in U87 cells. MTT and Transwell assays were applied to detect the decreased proliferation (a, b) and invasiveness (c, d). Columns: mean numbers. Bars: S.D. (*: P < 0.05; **: P < 0.01; ***: P < 0.001). e, f After transfection of the ZNF326 plasmid in the HEK293 cell line, immunoprecipitation and immunoblotting showed a significant decrease in the level of total β-catenin acetylation in a dose-dependent manner (e). ZNF326 overexpression in U87 also significantly decreased β-catenin acetylation at Lys49 (f); total β-catenin served as a loading control. g Wild-type ZNF326 deregulated the acetylation level at Lys49 and the phosphorylation level at Ser45 of β-catenin, while the mutant (both zinc-finger structures deleted) abrogated this effect; total β-catenin served as a loading control. h, i Co-transfection of ZNF326 and siRNA-HDAC7 or TSA added (10 nM) in U87 (h) and U251 cells (i), the downregulation of β-catenin acetylation level at Lys49 and phosphorylation level at Ser45 induced by ZNF326 were abrogated; total β-catenin served as the loading controlBack to article page