MAF Amplification licenses Estrogen Receptor a to Drive Breast Cancer Metastasis [dataset 1]
We performed mRNA profiling of control and MAF-overexpressing MCF7 cells to assess the transcriptional consequences of estrogen receptor (ER) activation upon metastatic MAF expression in the presence or absence or ER (using a protac for ER degradation). To this end, we cultured MCF7 cells in hormone-deprived (HD) medium for 72 h. At this point, we treated the cells with vehice or ER-protac for 24h and then estrogen (E2) or vehicle was added for 6h prior to RNA extraction. Samples were generated in triplicate. We report that MAF supports the expression of genes involved in metastatic functions and that E2 treatment and ER expression correlates with E2 early and late gene responses and cell cycle regulation. Additionally, a set of MAF and ER-dependent gene responses was identified. Our results show that MAF expression causes an expansion of ER-mediated transcriptional events in MCF7 cells exposed to E2. Overall design: To assess gene expression changes governed by MAF and estrogen receptor (ER), control or MAF-overexpressing MCF7 cells were maintained in hormone-deprived medium for 72 h. Then, ER-protac or vehicle was added for  24h. The day after E2 or vehicle was added for 6h prior to RNA extraction and mRNA profiling.