Fig. 6.

Effect of LAMP-2A and N-CoR expression on UPR activation and the apoptosis pathway in U87-MG cells. a UPR activation was examined by protein expression of p-PERK, p-IRE1, p-JNK and CHOP. LAMP-2A ablation resulted in remarkably increased expression of p-PERK, p-IRE1, p-JNK and CHOP, while N-CoR knockdown achieved opposite effect. These data together with findings from clinical samples, implied that CMA activation played important role in glioblastoma survival by degrading N-CoR and inhibiting downstream UPR activation. b Activator proteins in apoptosis including caspase 3, caspase 9 and Bax, and anti-apoptotic protein Bcl-2 were measured by western blot in differently treated U87-MG cells. Significant up-regulation of caspase 3, caspase 9 and Bax with simultaneous down-regulation of Bcl-2 were observed when LAMP-2A was inhibited, and these pro-apoptotic effects were reversed by N-CoR knockdown. The data are mean ± SEM from three independent experiments. The levels of p-PERK, p-IRE1 and p-JNK are compared with levels of PERK, IRE1 and JNK respectively, while the rest of the proteins are compared with β-actin. Protein levels are expressed relative to vehicle treatment group set as 1. Significant changes are set as p < 0.05 and represented by asterisk (One-Way ANOVA; Bonferroni's test)