Fig. 6

ERα-36 regulates progesterone-mediated cell proliferation. a T47D clones were plated onto 96-well plates and treated with R5020 (10 nM) or ethanol, and proliferation was measured using the IncuCyte technology. Image acquisition was conducted every hour using the IncuCyte software, which calculates the percentage of cell confluency as a function of time over 7 days. The results are represented as graphs showing the rate of proliferation every 24 h. The mean ± SD of one experiment representative of three experiments is shown. b The same experiment was performed, but the cells were steroid-deprived and treated with E2 (10 nM), R5020 (10 nM), or both. c Wound healing assays were performed in T47D clones WT or KO for ERα-36 as described in the “Methods” section. The percent of migration was determined as the mean of the distance of the wound for the different experiments. The analysis was performed in three separate experiments. Data are represented as means ± SEM from three replicates in each of the three independent experiments. *p < 0.05; ns, non-significant. d Using the wound healing assay performed in c, the relative migration R5020-dependent was calculated as the mean ± SEM for the three independent experiments. *p < 0.05. e Model of ERα-36 regulation of PR signaling. Upon progesterone treatment, ERα-36 activates a kinase involved in the phosphorylation of PR at S294 and S345 residues. ERα-36 could participate in coregulator recruitment to regulate PR transcriptional activity in a gene-dependent manner, which in turn modulates cell proliferation and migration. CoR, coregulators