AR ChIP-seq with DHT induction and GSK treatment

The major pioneer factor activity of FOXA1 in PCa is to facilitate AR recruitment to androgen-regulated enhancers. Therefore, we hypothesized that the decreased FOXA1 binding and enhancer availability by LSD1 inhibition may result in the impairment of subsequent AR recruitment to enhancers. To globally test this hypothesis, we performed AR ChIP-seq in LNCaP cells treated with an LSD1 inhibitors. Consistent with previous reports, DHT treatment can dramatically induce AR binding to chromatin. Significantly, LSD1 inhibitor treatment in presence of DHT stimulation markedly decreased the total number of AR binding peaks and their intensity. We further assessed the impact of LSD1 inhibition on overall AR transcriptional output using RNA-seq data. Overall design: AR ChIP-Seq were performed in LNCaP cells treated with vehicle, DHT (10nM at 4h), DHT (4h) with pretreated GSK2879552 (50µM for 4h), or DHT (4h) with pretreated GSK2879552 (48h)