We have used chromatin immunoprecipitation (ChIP) assay to follow transcription factor loading and monitor changes in covalent histone modifications associated with the prostate-specific antigen and kallikrein (KLK2) genes in response to androgen and antiandrogen in LNCaP cells. The dynamics of testosterone (T)-induced loading of androgen receptor (AR) onto the proximal promoters of the genes differed significantly from that onto the distal enhancers. Significantly more holo-AR was loaded onto the enhancers than the promoters, but the receptor’s residence time was more transient on the enhancers. Even though holo-AR recruited some RNA polymerase II (Pol II) onto the enhancers, the principal Pol II transcription complex was assembled on the promoters. The pure antiandrogen bicalutamide (CDX) complexed to AR elicited occupancy of the prostate-specific antigen promoter, but not that of the enhancer, whereas the partial antagonists cyproterone acetate (CPA) and mifepristone (RU486) were capable of promoting AR loading also onto the enhancer. In contrast THE ANDROGEN RECEPTOR (AR), a member of the nuclear receptor superfamily that functions as a ligand-regulated transcription factor, mediates a variety of developmental processes that create the male phenotype (1, 2). AR is a central player both in the development and maintenance of normal prostate as well as in the initiation and progression of prostate Abbreviations: AR, Androgen receptor; ARE, androgen response element; CARM1, coactivator-associated arginin
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