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 6. MCF7-Y537S cells show a significant increase in mitochondrial oxygen consumption rate (OCR) and ATP production. The Seahorse XFe96 metabolic-flux analyzer was employed to determine mitochondrial function in all of the MCF7 cell transfectants, after 48 hours of pre-treatment with 4-OHT (1 µM). (Panel A) A representative line graph of 3 independent experiments is shown (+/- SEM). (Panels B, C and D) Note that respiration (basal and maximal), as well as ATP levels, were significantly increased in MCF7-Y537S and MCF7-Y537N cells. However, MCF7-Y537S cells showed that largest increases. ** p < 0.001; **** p < 0.00001; ns = not significant.