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. 2021 Oct 20;12(11):975. doi: 10.1038/s41419-021-04212-7

Fig. 2. Absence of EZH2 in glucose-sensitive CRCs enhanced the tolerance to glucose-deprivation-induced cell death.

Fig. 2

A, B Representative images of HCT116 (A) or RKO (B) NC and shEZH2 cells under normal condition or glucose deprivation. The experiments were repeated twice independently with similar results. C Immunoblotting for EZH2 knockdown efficiency in RKO and HCT116 cells. Actin is used as a loading control. D, E Immunoblotting for cleaved-PARP and EZH2 expression in HCT116 (D) or SW480 (E) NC and shEZH2 cells under normal condition or glucose deprivation (0 mM, 16 h). F, G Immunoblotting for cleaved-PARP and H3K27me3 expression in HCT116 (F) or SW480 (G) cells pretreated with or without GSK126 (4 μM, 48 h), followed by glucose deprivation treatment (0 mM, 12 h). H Immunoblotting for cleaved-PARP and EZH2 expression in HCT116 cells with or without EZH2 overexpression under normal condition or glucose deprivation. I, J Living cell counting of HCT116 (I) or SW480 (J) NC and shEZH2 cells under normal condition or glucose deprivation (0 mM, 20 h). K Living cell counting of HCT116 cells pretreated with or without GSK126 (4 μM, 72 h), cultured under normal condition or glucose deprivation (0 mM, 20 h). The experiments in C–H were repeated twice independently with similar results. In I, J, K, data are mean ± s.d., n = 3 independent experiments; P-values were calculated using two-tailed unpaired Student’s t-test. *P < 0.05, **P < 0.01, ***P < 0.001. Scale bars, 200 μm.