Transcription profiling of human LNCaP prostate cancer cells to investigate the effect of HDAC inhibitors on expression of androgen induced genes

ABSTRACT: Elevated levels of androgen receptor (AR) in prostate cancer confer resistance to current antiandrogens and play a causal role in disease progression due to persistent target gene activation. Through pharmacologic and genetic approaches, we show that half of all direct AR target genes, including TMPRSS2, the primary driver of ETS fusion transcripts in 70 percent of human prostate cancers, require histone deacetylase (HDAC) activity for transcriptional activation by AR. Surprisingly, the HDAC3-NCoR complex, which typically functions to repress gene expression by nuclear receptors, is required for AR target gene activation. Prostate cancer cells treated with HDAC inhibitors have reduced AR protein levels, but we show that the mechanism of blockade of AR activity is through failure to asse

ORGANISM(S): Homo sapiens

SUBMITTER: Yu Chen 

PROVIDER: E-GEOD-9000 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress