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. 2013 Jul 18;8(7):e68614. doi: 10.1371/journal.pone.0068614

Figure 3. Inactivation of GSK3β upregulated EZH2 production in NPC cells.

Figure 3

(A) The transfection efficiency was evaluated by testing the protein level of GSK3β. Representative western blot analysis of p-GSK3β (Ser9) after GSK3β-CA or KD transfection or lithium treatment (20 mmol/L) in NPC cells; (B) GSK3β-CA transfection (2 μg/mL) significantly reduced p-GSK3β (Ser9) production in CNE-1 and CNE-2 cells, whereas GSK3β-KD transfection (2 μg/mL) or lithium treatment (20 mmol/L) significantly increased p-GSK3β (Ser9) production in CNE-1 and CNE-2 cells; (C) Representative western blot analysis of EZH2 after GSK3β-CA or KD transfection in NPC cells; (D) GSK3β-CA transfection (2 μg/mL) significantly reduced EZH2 production in CNE-1 and CNE-2 cells, whereas GSK3β-KD transfection (2 μg/mL) significantly increased EZH2 production in CNE-1 and CNE-2 cells; (E) Representative western blot analysis of EZH2 after lithium treatment (20 mmol/L) in NPC cells; (F) Lithium treatment (20 mmol/L) significantly increased EZH2 production in CNE-1 and CNE-2 cells. The data indicate the means (SEM) of 3 independent experiments. NC: normal control; CA: constitutively active GSK-3β plasmid; KD: kinase-dead GSK-3β plasmid.