MAF Amplification licenses Estrogen Receptor a to Drive Breast Cancer Metastasis [dataset 2]
We mapped chromatin accessibility on control and MAF-overexpressing MCF7 cells to assess the consequences of estrogen (E2, estrogen cepetor (ER) and metastatic MAF expression on the chromatin landscape. To this end, we cultured MCF7 cells in hormone-deprived (HD) medium for 72 h and a specific ER-protac or vehicle was added for 24h for ER degradation.  The day after, estrogen (E2) or vehicle was added for 1h prior to DNA purification. Samples were generated in duplicate. We report changes in chromaitn accessibility depending on both MAF expression and E2 stimulation. Overall design: In order to assess changes in chromatin accessibility governed by MAF, ER and estrogen (E2), control or MAF-overexpressing MCF7 cells were maintained in hormone-deprived medium for 72 h. Then, an ER-protac or vehicle was added for 24h and cells were stimulated with E2 or vehicle for 1h. DNA was purified for ATAC-seq analysis