Fig. 6

Nuclear TKT promotes the proliferation, viability, and migration of HCC cells in a non-metabolic manner and predicts a poor prognosis of HCC patients. a TKT overexpressing stable cell lines, including TKT wild type, TKT-Y4A, TKT-K6R, TKT-D155A, TKT-D155A-Y4A, TKT-D155A-K6R in Huh7 and HepG2 cells were established and validated by western blot. b Proliferation rates of TKT wild type, TKT-Y4A and TKT-K6R with or without the D155A dominant-negative mutation in Huh7 and HepG2 cells. c Viability of TKT wild type, TKT-Y4A and TKT-K6R with or without the D155A dominant-negative mutation in Huh7 and HepG2 cells under oxidative stress. Cells were treated with H₂O₂ for 6 h. d Migration of TKT wild type, TKT-Y4A and TKT-K6R with or without the D155A dominant-negative mutation in Huh7 and HepG2 cells. e The association of nuclear TKT level with OS and DFS of HCC patients (n = 286, Kaplan–Meier analysis, p value from log-rank test). Upper: OS data set; lower: DFS data set. nTKT/cTKT, the nuclear TKT to the cytoplasmic TKT ratio. Low, nTKT/cTKT ratio < 1, n = 96. High, nTKT/cTKT ratio ≥ 1, n = 190. Nuclear and cytoplasmic TKT levels were scored by IHC (*: p < 0.05; **: p < 0.01)