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Fig. 2 | Journal of Experimental & Clinical Cancer Research

Fig. 2

From: Mediation of PKM2-dependent glycolytic and non-glycolytic pathways by ENO2 in head and neck cancer development

Fig. 2

ENO2 promotes cell proliferation and glucose metabolism in HNSCC cells. a Effect of ENO2 knockdown on AKT and ERK1/2 signaling pathways in UM-1 and Cal27 cells determined by western blotting. b-d Effect of ENO2 knockdown on cell proliferation (b), colony formation (c) and anchorage-independent growth (d) in UM-1 and Cal27 cells determined by MTT, clonogenic and soft agar assays, respectively. € Effect of ENO2 overexpression on AKT and ERK1/2 signaling pathways in Cal33 and HSC3 cells determined by western blotting. f-h Effect of ENO2 overexpression on cell proliferation (f), colony formation (g) and anchorage-independent growth (h) in Cal33 and HSC3 cells determined by MTT, clonogenic and soft agar assays, respectively. i Effect of ENO2 knockdown on the cellular levels of ATP and glucose in UM-1 and Cal27 cells determined by ATP assay kit and Glucose Uptake-Glo assay kit, respectively. j Effect of ENO2 overexpression on the cellular levels of ATP and glucose uptake in Cal33 and HSC3 cells determined by ATP assay kit and Glucose Uptake-Glo assay kit, respectively. k Effect of ENO2 knockdown on the cell cycle progression in UM-1 and Cal27 cells determined by flow cytometry with PI staining. The quantitative data are shown in the right panel. l Effect of ENO2 knockdown on cell cycle-related protein expression in UM-1 and Cal27 cells determined by western blotting. The quantitative data are shown in the right panel. *p<0.05; **p<0.01

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