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Abstract: The progression of prostate cancer is largely dependent on the activity of the androgen receptor (AR), which in turn, correlates with the net output of the AR transcriptional regulatory network. A detailed and thorough understanding of the AR transcriptional regulatory network is therefore critical in the strategic manipulation of AR activity for the targeted eradication of prostate cancer cells. In this mini-review, we highlight some of the novel and unexpected mechanistic and functional insights of the AR transcriptional network derived from recent targeted sequencing (ChIP–Seq) studies of AR and its coregulatory factors in prostate cancer cells. [Copyright &y& Elsevier]

Oestrogen receptor ? (ER?) is key player in the progression of breast cancer. Recently, the cistrome and interactome of ER? were mapped in breast cancer cells, revealing the importance of spatial organization in oestrogen-mediated transcription. However, the underlying mechanism of this process is unclear. Here, we show that ER? binding sites (ERBS) identified from the Chromatin Interaction Analysis-Paired End DiTag of ER? are enriched for AP-2 motifs. We demonstrate the transcription factor, AP-2?, which has been implicated in breast cancer oncogenesis, binds to ERBS in a ligand-independent manner. Furthermore, perturbation of AP-2? expression impaired ER? DNA binding, long-range chromatin interactions, and gene transcription. In genome-wide analyses, we show that a large number of AP-2? and ER? binding events converge together across the genome. The majority of these shared regions are also occupied by the pioneer factor, FoxA1. Molecular studies indicate there is functional interplay between AP-2? and FoxA1. Finally, we show that most ERBS associated with long-range chromatin interactions are colocalized with AP-2? and FoxA1. Together, our results suggest AP-2? is a novel collaborative factor in ER?-mediated transcription. [ABSTRACT FROM AUTHOR]