Skip to main content
Fig. 3 | Cancer Cell International

Fig. 3

From: TET2 suppresses nasopharyngeal carcinoma progression by inhibiting glycolysis metabolism

Fig. 3

TET2-PKM interaction is required for TET2 inhibiting proliferation and invasion of NPC cells. a Flag-TET2 was immunoprecipitated and examined by western blotting. b Endogenous TET2 interacting with PKM was detected by protein immunoprecipitation in CNE1 and SUNE1 cells. c Exogenous TET2 interacting with PKM was detected by protein immunoprecipitation in CNE1 cells. d Full length (FL) TET2 or different truncations of TET2 interacting with PKM was detected by protein immunoprecipitation in CNE1 cells (N: N-terminal TET2, residues 1–1127 amino acids; C1: C1-terminal TET2, residues 1128–2002 amino acids; C2: C2-terminal TET2, residues 1399–2002 amino acids; DSBH: double-strand beta helix domain of TET2, residues 1868–2002 amino acids). Cell viability (e) and cell invasive ability (f) of CNE1 cells transfected with the indicated plasmids were examined. Cell viability (g) and cell invasive ability (h) of CNE1 cells transfected with the indicated plasmids and siR-PKM were examined. Data are represented as mean ± SD (n = 3; *represents P < 0.05)

Back to article page
\