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Androgen deprivation therapy for prostate cancer (PCa) benefits patients with early disease, but becomes ineffective as PCa progresses to a castration-resistant state (CRPC). Initially CRPC remains dependent on androgen receptor (AR) signaling, often through increased expression of full-length AR (ARfl) or expression of dominantly active splice variants such as ARv7. We show in ARv7-dependent CRPC models that ARv7 binds together with ARfl to repress transcription of a set of growth-suppressive genes. Expression of the ARv7-repressed targets and ARv7 protein expression are negatively correlated and predicts for outcome in PCa patients. Our results provide insights into the role of ARv7 in CRPC and define a set of potential biomarkers for tumors dependent on ARv7.
Pubmed ID: 30773341 RIS Download
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This polyclonal targets NCOR2
View all literature mentionsThis polyclonal targets FOXA1 antibody - ChIP Grade
View all literature mentionsThis polyclonal targets H3K27ac
View all literature mentionsThis monoclonal secondary targets IgG, Light Chain Specific
View all literature mentionsThis unknown targets AR (ARv7 Splice Variant)
View all literature mentionsThis monoclonal targets Raised against amino acids 299-315 of AR of human origin.
View all literature mentionsThis polyclonal targets Foxa1
View all literature mentionsThis unknown targets NCoR1
View all literature mentionsThis monoclonal secondary targets IgG, Light Chain Specific
View all literature mentionsThis monoclonal targets Raised against amino acids 299-315 of AR of human origin.
View all literature mentionsThis unknown targets NCoR1
View all literature mentionsThis unknown targets AR (ARv7 Splice Variant)
View all literature mentionsThis polyclonal targets FOXA1 antibody - ChIP Grade
View all literature mentionsThis polyclonal targets H3K27ac
View all literature mentionsThis polyclonal targets Foxa1
View all literature mentionsThis polyclonal targets NCOR2
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