Figure 2
(A–C) Relative changes in (A) glutamine consumption, (B) α-KG production and (C) intracellular ATP content in BxPC-3, PANC-1 and AsPC-1 cells upon ASCT2 knockdown (*P<0.05, **P<0.01, versus the control group). (D–F) Relative changes in (D) glutamine consumption, (E) α-KG production and (F) intracellular ATP content in BxPC-3, PANC-1 and AsPC-1 cells in the presence of the ASCT2 inhibitor GPNA (2 mM) (*P<0.05, **P<0.01, versus the control group). (G,H) Relative changes in (G) intracellular ATP content, (H) ROS generation for control or shASCT2 in the presence or absence of NAC in BxPC-3, PANC-1 and AsPC-1 cells (*P<0.05, **P<0.01, versus the control group or shASCT2).
Effect of ASCT2 knockdown or chemical inhibition on cell glutamine metabolism in BxPC-3, PANC-1 and AsPC-1 cells

(A–C) Relative changes in (A) glutamine consumption, (B) α-KG production and (C) intracellular ATP content in BxPC-3, PANC-1 and AsPC-1 cells upon ASCT2 knockdown (*P<0.05, **P<0.01, versus the control group). (D–F) Relative changes in (D) glutamine consumption, (E) α-KG production and (F) intracellular ATP content in BxPC-3, PANC-1 and AsPC-1 cells in the presence of the ASCT2 inhibitor GPNA (2 mM) (*P<0.05, **P<0.01, versus the control group). (G,H) Relative changes in (G) intracellular ATP content, (H) ROS generation for control or shASCT2 in the presence or absence of NAC in BxPC-3, PANC-1 and AsPC-1 cells (*P<0.05, **P<0.01, versus the control group or shASCT2).

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