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 5. MCF7-Y537S cells show increased ALDH activity, which is resistant to Tamoxifen treatment. All the transfected MCF7 cell lines were first grown as mammospheres and then used to prepare a single-cell suspension, which was subjected to “stemness” assays with ALDEFLOUR, to measure ALDH activity. Importantly, only Y537S cells show significant increases (>3-fold) in ALDH activity. Also, note that treatment with 4-OHT (1 µM) inhibits ALDH activity in empty vector (EV) control cells, but not in MCF7-Y537S cells. * p< 0.05; *** p< 0.0005; ns = not significant, as evaluated by Student’s t test. (Panel A) ALDH activity; (Panel B) ALDH activity, with and without treatment with 4-OHT. This observation is consistent with the idea that increased stemness helps to confer tamoxifen-resistance.