Fig. 4

CircRNF13 inhibits glycolysis in NPC cells. A Glucose consumption and lactate production in HNE2 and CNE2 cells were examined using an automated biochemical analyzer, upon circRNF13 overexpression. Data have been represented as mean ± SD from three independent experiments. *, p < 0.05. B The extracellular acidification rate (ECAR) in HNE2 and CNE2 cells was measured using Seahorse XF assay, in response to circRNF13 overexpression or knockdown. Glycolysis, glycolytic capacity, and glycolytic reserve were analyzed. Data have been represented as mean ± SD. *, p < 0.05; **, p < 0.01. C Expression levels of downstream targets of phosphorylated AMPKα and mTOR, S6K and 4EBP1, were measured using western blotting in HNE2 and CNE2 cells in response to circRNF13 overexpression or knockdown. D Expression levels of downstream targets of phosphorylated AMPKα and mTOR, S6K and 4EBP1, were measured using western blotting in HNE2 and CNE2 cells treated with the glycolysis inhibitor 2-DG, in response to circRNF13 overexpression or knockdown. E The glycolysis inhibitor 2-DG attenuated the effect of circRNF13 on NPC cell migration in HNE2 and CNE2 cells transfected with sicircRNF13, as assessed using wound-healing assay. All experiments were repeated at least three times. Data have been represented as mean ± SD. ***, p < 0.001. F The glycolysis inhibitor 2-DG weakened the function of circRNF13 on NPC cell invasion when HNE2 and CNE2 cells transfected with sicircRNF13 were treated with the glycolysis inhibitor 2-DG, as assessed using Transwell assays. All experiments were repeated at least three times. Data have been represented as mean ± SD. ***, p < 0.001