Fig. 5
From: Loss of hexokinase 1 sensitizes ovarian cancer to high-dose metformin
The catalytically dead variant of HK1. a Position of p.D656A and p.T657A variations in HK1, PDB structure 1HKB [36]. b KM and Vmax as measured in vitro for the WT HK1 and its p.D656A and p.T657A variations. c Relative alamarBlue absorbance generated by the HK1− or HK2− TOV-112D cells, HK1 and HK2 revertants and HK1 D656A knock-in in TOV-112D cells that were cultivated for 24 h in DMEM with 5.5 mM or 0.4 mM glucose or with 5.5 mM fructose in the presence or absence of 2 mM metformin. The data are displayed relative to alamarBlue absorbance of each respective cell clone in the respective condition without metformin. d–f The NADPH/NADP ratios (d), glutathione levels (e), and NAD/NADH ratios (f) in metformin-treated HK1− or HK2− TOV-112D cells, HK1 and HK2 revertants, and HK1 D656A knock-in in TOV-112D cells that were cultivated in DMEM with 0.4 mM glucose for 36 h. g The NADPH/NADP ratios HK1− TOV-112D cells, HK1 revertants, and HK1 D656A knock-in in TOV-112D cells that were cultivated in DMEM without glucose and with dialyzed serum, with or without 2 mM metformin for 36 h. h Targeted GC×GC-MS analysis of changes in metabolites induced by changes in HK1 and HK2 in TOV-112D cells. Data are shown as relative values, where red indicates maximum concentration and blue indicates the lowest concentration of the respective metabolite in the six analyzed cell clones