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 1. Lentiviral transduction with the ESR1 (Y537S) mutation is sufficient to stably confer Tamoxifen-resistance in MCF7 cell monolayers: Effects on cell viability. Briefly, MCF7 cells were stably-transduced with either ESR1 (WT, Y537S, or Y537N) or ErbB2 (HER2), to genetically create a clinically relevant model of hormone therapy resistance. Vector alone control MCF7 cells were generated in parallel (empty vector; EV; p-EV-105-puroR), as a negative control. Importantly, note that MCF7-Y537S cells clearly show resistance to 4-OHT (1 µM). The SRB assay was performed as a measure of cell viability and the experiment was carried out for 5 days. In contrast, 4-OHT has significant inhibitory effects on the viability of the other MCF7 cell lines. ** p<0.005.