Fig 1: Effect of ß-oxidation and glucose metabolism on the phenotype of 17ß-HSD12 silencing. a Number of MDA-MB-231 cells counted 48 h post mock- or 17ß-HSD12-siRNA transfection and 24 h after treatment with the inhibitor of mitochondrial ß-oxidation Eto (top, n = 6) or peroxisomal ß-oxidation Thio (bottom, n = 5) (mean ± SD, *p < 0.05, ns not significant). b ECAR was measured for MDA-MB-231 and SUM159 cells at baseline using the Seahorse XF96 analyzer during the experiments described in Fig. 5 (mean ± SD, n = 5, **p < 0.01, ns not significant). The statistical analysis depicted in blue characters compared the differences in the values between the corresponding mock siRNA and 17ß-HSD12 siRNA samples. c Cells counted after knockdown of 17ß-HSD12 in MDA-MB-231 (n = 4) and SUM159 (n = 5) cells and culturing in RPMI 1640 medium-containing 4 g/l, 2 g/l or 0.5 g/l glucose. The dotted lines represent the statistical comparison between the different mock siRNA/17ß-HSD12 siRNA groups, whereas the solid lines constitute comparison between the indicated mock siRNA and 17ß-HSD12 siRNA samples (mean ± SD, *p < 0.05, **p < 0.01, ***p < 0.01, ns not significant). d The levels of G6PD in MDA-MB-231 and SUM159 cells were assessed by western blot and quantified by densitometry (mean ± SD, n = 4, *p < 0.05, ns not significant)