Targeting the MLL complex in castration-resistant prostate cancer [ChIP-seq]

ABSTRACT: Men who develop metastatic castration-resistant prostate cancer (CRPC) invariably succumb to the disease. The development and progression to CRPC following androgen ablation therapy is predominantly driven by unregulated androgen receptor (AR) signaling. Despite the success of recently approved therapies targeting AR signaling, such as abiraterone and second-generation anti-androgens MDV3100 (enzalutamide), durable responses are limited, presumably due to acquired resistance. Recently, JQ1 and I-BET, two selective small molecule inhibitors that target the amino-terminal bromodomains of BRD4, have been shown to exhibit antiproliferative effects in a range of malignancies. Here we show that AR signaling-competent CRPC cell lines are preferentially sensitive to BET bromodomain inhibition. BRD

ORGANISM(S): Homo sapiens

SUBMITTER: Marcin Cieslik 

PROVIDER: E-GEOD-60841 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress