Fig. 6: GLS is involved in the resistance of EZH2-deficient cells to glucose deprivation.
From: Tumor-suppressive function of EZH2 is through inhibiting glutaminase
A, B Immunoblotting for cleaved-PARP and GLS expression in HCT116 (A) or SW480 (B) cells pretreated with or without GSK126 (4 μM, 48 h) or/and BPTES (10 μM, 48 h), followed by glucose deprivation treatment (0 mM, 16 h). Actin is used as a loading control. C, D Immunoblotting for cleaved-PARP and GLS expression in HCT116 NC and shEZH2 cells (C) or SW480 NC and shEZH2 cells (D) cells pretreated with DMSO or BPTES (10 μM, 48 h), followed by glucose deprivation treatment (0 mM, 16 h). E Three-day growth of HCT116 NC and shEZH2 cells or SW480 NC and shEZH2 cells in presence or not of 5 μM BPTES. F Growth curves of HCT116 or SW480 cells in presence or not of 2 μM GSK126 or/and 5 μM BPTES. G, H Colony formation of HCT116 (G) or SW480 (H) cells in presence or not of 2 μM GSK126 or/and 5 μM BPTES. The experiments in A–D and G, H were repeated twice independently with similar results. In E, F, data are mean ± s.d., n = 3 independent experiments; P-values were calculated using two-tailed unpaired Student’s t-test or two-way ANOVA test. *P < 0.05, **P < 0.01, ***P < 0.001.
