Research Paper Volume 10, Issue 12 pp 4000—4023
The ER-alpha mutation Y537S confers Tamoxifen-resistance via enhanced mitochondrial metabolism, glycolysis and Rho-GDI/PTEN signaling: Implicating TIGAR in somatic resistance to endocrine therapy
Figure 7. MCF7-Y537S cells show a significant increase in extracellular acidification rate (ECAR) and glycolysis levels. The Seahorse XFe96 metabolic-flux analyzer was employed to determine the metabolic function of all transfected cells after 48 hours of treatment with 4-OHT (1 µM). (Panel A) A representative line graph of 3 independent experiments is shown (+/- SEM). (Panel B) Glycolysis was significantly increased only in MCF7-Y537S cells and reduced in MCF7-ErbB2 and MCF7-ESRI cells. (Panel C) Glycolytic capacity was significantly increased only in MCF7-Y537S and reduced in MCF7-ErbB2 and MCF7-ESRI cells. (Panel D) Glycolytic reserve capacity was significantly increased only in MCF7-Y537S cells. ** p < 0.001; *** p 0.0001; **** p < 0.00001; ns = not significant.