Inhibition of GSK 3β Activity Is Associated with Excessive EZH2 Expression and Enhanced Tumour Invasion in Nasopharyngeal Carcinoma
Figure 4
GSK3β inactivation promoted the stability of EZH2 protein in vitro.
(A, B) Representative western blot analysis of EZH2 after GSK3β-KD (2 μg/mL) or control plasmid transfection in CNE-1 cells; CNE-1 cells were treated with cycloheximide (20 μM) after transfection, and EZH2 protein level in the indicated time point was detected by western blot analysis which containing equal amounts of protein. (C) The half-life of EZH2, as suggested by the relative EZH2 intensity, was significantly longer in GSK3β-KD group than in normal control (p<0.05). The data indicate the means (SEM) of 3 independent experiments. KD: kinase-dead GSK3β plasmid; NC, normal control plasmid.