GSE61838
Genome-wide analysis of full-length Androgen Receptor (AR) and AR Splice Variant (ARv567es) cistromes
Androgen Receptor (AR) variants (AR-V) drive prostate cancer (PCa) resistance to first and second-generation therapies targeting endocrine regulation of AR. To understand the sets of genomic targets of full-length AR vs. AR-Vs, we conducted genome-wide ChIP-seq using isogenic pairs of genome engineering cell lines expressing either ARv567es (R1-D567) or full-length AR (R1-AD1).  Our data demonstrate that androgen-activated full-length AR and AR-Vs both bind to similar genomic targets, which are enriched for high affinity androgen response elements (AREs).  Overall, this study demonstrates that AR-Vs restore the broad AR cistrome that is otherwise lost during endocrine-targeted therapy. Overall design: ChIP-Seq of full-length Androgen Receptor (AR)  or AR splice variant (ARv567es) binding to genomic DNA