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Series GSE28950 Query DataSets for GSE28950
Status Public on Apr 27, 2012
Title TMPRSS2-ERG, HDACs and EZH2 are involved in an AR-centric transcriptional circuitry that calibrates androgenic response for prostate cancer progression (ChIP-Seq data)
Organism Homo sapiens
Experiment type Genome binding/occupancy profiling by high throughput sequencing
Summary Deregulation of the Androgen Receptor (AR) transcriptional network is a common hallmark in prostate cancers. To achieve its precise transcriptional role, AR needs to co-operate specifically with a plethora of cofactors. In prostate cancers, AR transcription collaborators are frequently aberrantly over-expressed, altering the AR signaling pathway to one that promotes oncogenesis. Recently, the prostate cancer recurrent fusion gene, ERG, was shown to promote tumor progression by acting as a repressor of AR signaling. However, the exact mechanics and the functional consequences associated with this crosstalk between ERG and AR still remains relatively unknown. Interestingly, through chromatin immunoprecipitation coupled with massively parallel sequencing, we discover that ERG and other commonly over-expressed transcriptional co-repressors (HDAC1, HDAC2, HDAC3 and EZH2) are wired into an AR-centric transcriptional network via a spectrum of distal enhancers and/or proximal promoters. We show that ERG represses several AR target genes involved in epithelial differentiation. Furthermore, we demonstrated that suppression of the androgen-induced gene, Vinculin, by ERG and histone deacetylases increases cancer cell invasiveness. From our results, we propose that ERG, histone deactelyases and the histone methyltransferase, EZH2, could impede epithelial differentiation and contribute to prostate cancer progression, in part through modulating the transcriptional output of AR.
Overall design Genome-wide binding analysis of AR, ERG, HDAC1, HDAC2, HDAC3 and EZH2 in VCaP with and without DHT (dihydrotestosterone) stimulation using ChIP-Seq. 15 samples including 1 control (input).
Contributor(s) Chng KR, Chang CW, Tan SK, Yang C, Hong SZ, Cheung E
Citation(s) 22531786
Submission date Apr 28, 2011
Last update date May 15, 2019
Contact name Kern Rei Chng
Organization name GIS
Department Cancer Biology and Pharmacology 3
Lab Cancer Biology and Pharmacology 3
Street address 60 Biopolis Street #02-01 Genome
City Singapore
ZIP/Postal code 138672
Country Singapore
Platforms (1)
GPL9115 Illumina Genome Analyzer II (Homo sapiens)
Samples (15)
GSM717391 VCaP Genomic Input sequencing
GSM717392 AR ChIP sequencing in 0hr treated VCaP cells
GSM717393 AR ChIP sequencing in 2hr 100nM DHT treated VCaP cells
This SubSeries is part of SuperSeries:
GSE28951 TMPRSS2-ERG, HDACs and EZH2 are involved in an AR-centric transcriptional circuitry that calibrates androgenic response for prostate cancer progression
SRA SRP006579
BioProject PRJNA142869

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE28950_RAW.tar 3.4 Gb (http)(custom) TAR (of BED, TXT)
SRA Run SelectorHelp
Raw data are available in SRA
Processed data provided as supplementary file

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