Fig. 2: Chromatin-immunoprecipitation sequence (ChIP seq) using antibody against androgen receptor (AR).

a Top: Experimental schemes. KUCaP tumors under androgen-dependent (AD) and castration-resistant (CR) growth were obtained. Bottom: LNCaP cells cultured in FBS, charcoal-strip FBS (CSFBS) and CSFBS supplemented with 1 nM dihydrotestosterone (CSFBS + DHT) as well as AILNCaP cultured in CSFBS were subject to CHiP seq. b Quality controls for ChIP seq binding data. Bar files were generated after MAT analysis of AR whole-genome ChIP seq raw data from LNCaP cells cultured in FBS, charcoal-strip FBS (CSFBS), and CSFBS supplemented with 1 nM dihydrotestosterone (DHT). AR-binding peaks at the promoter regions (unless otherwise indicated) of indicated genes¹³ are shown. KLK3 p; KLK3 (PSA) promoter, KLK3 e; KLK3 (PSA) enhancer, FKBP5 3', 3' UTR region of FKBP5. c Venn diagrams showing AR-binding sites in KUCaP2 AD and CR tumors (top), and LNCaP and AILNCaP cells (bottom). We identified 3131 differential AR-binding sites for KUCaP AD tumors, 1850 for KUCaP2 CR tumors, 2,938 for LNCaP cells, and 717 for AILNCaP cells, which were defined as having fold change ≤ 0.5 or ≥2 compared with each counterpart. There were 6102 AR-binding sites commonly identified in KUCaP2 AD and CR tumors and 1751 in LNCaP and AILNCaP cells. d Reactome pathways for genes exclusively identified for KUCaP2 CR tumors annotated by AR-binding sites in AR-ChIP seq with regard to entities p-values (−log[p-value]). e, f Venn diagrams depicting differentially and commonly identified genes harboring AR-binding site in AD (e) and CR (f) models including PDX (the present study), human PCa tissue²², and cell lines¹³.