Characterization of the AR cistrome in ER-negative breast cancer cell lines

Although molecular apocrine and some triple negative breast cancer tumours express high levels of AR, how AR signalling impacts their proliferative rate remains an area of controversy. The precise molecular mechanisms by which the AR can induce divergent proliferative effects in estrogen receptor-negative breast cancers has not been described. The potent androgen, DHT, inhibits proliferation of the MFM-223 estrogen receptor-negative breast cancer cell line. In contrast, activation of the AR by DHT either stimulates, or has no effect, on MDA-MB-453 cell proliferation. The AR cistrome was examined in order to identify candidate factors which mediate oncogenic versus tumour suppressive AR activity in ER-negative breast cancer. Overall design: Two cell line models of estrogen receptor-negative breast cancer; MDA-MB-453 and MFM-223; were cultured in steroid-deplete conditions and treated for 4 hours with either a vehicle (0.001% ethanol) or 10 nM DHT. Three replicate AR ChIP-seq experiments were performed, each corresponding to independent and consecutive passages of cells. One input file is provided for each cell line. Peak files are provided for each replicate, and one bigwig file is provided for each treatment, corresponding to a merge of the data from all 3 replicates.