Fig. 5.

TET2 interacting with PKM inhibits proliferation and invasion of NPC cells by suppressing glycolysis. a Glucose uptake or intracellular PH value in CNE1 cells (control) or TET2-knockout CNE1 cells (TET2-cas9) transfected with siR-NC (NC) or siR-PKM. b Lactate or PEP production in CNE1 cells (control) or CNE1 cells transfected with pcmv-flag-TET2 or pcmv-flag-TET2Δ with deficiency of catalytic activity, and treated with ATP (100 μmol/L) for 24 h was examined. c Lactate or PEP production in CNE1 cells (control) or CNE1 cells transfected with the indicated plasmids and treated with ATP (100 μmol/L) for 24 h was examined. d Lactate or PEP production in CNE1 cells (control) or TET2-knockout CNE1 cells (TET2-cas9) treated with ATP (5 mM) for 24 h was examined. e Lactate or PEP production in CNE1 cells (control) or TET2-knockout CNE1 cells (TET2-cas9) treated with PKM inhibitor, shikonin (10 μmol/L) for 24 h was examined. Cell viability (f) and cell invasive ability (g) of CNE1 cells (control) or TET2-knockout CNE1 cells (TET2-cas9) treated with the PKM inhibitor shikonin (10 μmol/L) or the glucose analog 2-deoxyglucose (2-DG, 5 mM) for 24 h was examined. Data are represented as mean ± SD (n = 3; *represents P < 0.05)