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Inhibition of BET bromodomain proteins as a therapeutic approach in prostate cancer

ABSTRACT: We analyzed transcriptional changes in 4 prostate cancer cell lines following treatment with the BET inhibitor I-BET762 using Affymetrix Human Genome U133 Plus 2.0 Arrays.

ORGANISM(S): Homo sapiens

PROVIDER: GSE56352 | GEO | 2014/03/31

SECONDARY ACCESSION(S): PRJNA243023

REPOSITORIES: GEO

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Inhibition of BET bromodomain proteins as a therapeutic approach in prostate cancer

Project description:We analyzed transcriptional changes in 4 prostate cancer cell lines following treatment with the BET inhibitor I-BET762 using Affymetrix Human Genome U133 Plus 2.0 Arrays. Four prostate cancer cell lines (NCI-H660, VCaP, LNCaP, PC-3) were treated with DMSO (control) or I-BET762 at 0.5uM or 10uM concentrations for 24 hours. Two biological replicates are included for each treatment group.

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Project description: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) signaling1-3. Despite the success of recently approved therapies targeting AR signaling such as abiraterone4-6 and second generation anti-androgens MDV3100 (enzalutamide)7,8, 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 malignancies9-12. Here we show that AR signaling-competent CRPC cell lines are preferentially sensitive to BET bromodomain inhibition. BRD4 physically interacts with the N-terminal domain of AR and can be disrupted by JQ111,13. Like the direct AR antagonist, MDV3100, JQ1 disrupted AR recruitment to target gene loci. In contrast to MDV3100, JQ1 functions downstream of AR, and more potently abrogated BRD4 localization to AR target loci and AR mediated gene transcription including induction of TMPRSS2-ERG and its oncogenic activity. In vivo, BET bromodomain inhibition was more efficacious than direct AR antagonism in CRPC xenograft models. Taken together, these studies provide a novel epigenetic approach for the concerted blockade of oncogenic drivers in advanced prostate cancer. Two-color experiment, in duplicates

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