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Androgen receptor RIME in prostate cancer cells

ABSTRACT: Androgen receptor (AR) is a master transcription factor that drives prostate cancer (PCa) development and progression. Alterations in the expression or activity of AR coregulators significantly impact the disease's outcome. To identify all the essential components of the AR coregulator complex, we utilized a proteomic approach called rapid immunoprecipitation of endogenous proteins (RIME) to systematically identify all coregulator proteins of the AR interactome in PCa cells.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Permanent Cell Line Cell, Cell Culture

DISEASE(S): Prostate Adenocarcinoma

SUBMITTER: mi chen

LAB HEAD: Edwin Chong Wing CHEUNG

PROVIDER: PXD031273 | Pride | 2022-07-12

REPOSITORIES: Pride

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			Action	DRS
	20170307_Sample_5.raw	Raw
	20170307_Sample_5SD.raw	Raw
	20170307_Sample_6.raw	Raw
	20170307_Sample_6SD.raw	Raw
	20170323_Sample11.raw	Raw

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Publications

TRIM33 drives prostate tumor growth by stabilizing androgen receptor from Skp2-mediated degradation.

Chen Mi M Lingadahalli Shreyas S Narwade Nitin N Lei Kate Man Kei KMK Liu Shanshan S Zhao Zuxianglan Z Zheng Yimin Y Lu Qian Q Tang Alexander Hin Ning AHN Poon Terence Chuen Wai TCW Cheung Edwin E

EMBO reports 20220704 8

Androgen receptor (AR) is a master transcription factor that drives prostate cancer (PCa) development and progression. Alterations in the expression or activity of AR coregulators significantly impact the outcome of the disease. Using a proteomics approach, we identified the tripartite motif-containing 33 (TRIM33) as a novel transcriptional coactivator of AR. We demonstrate that TRIM33 facilitates AR chromatin binding to directly regulate a transcription program that promotes PCa progression. TR ...[more]

PMID: 35785414

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Genome wide mapping of AR and its associated factors in prostate cancer

Project description:Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation.We performed ChIP-seq analysis to investigate the role of AR and its associated factors such as coregulators or collaborating factors.In addition, by siRNA mediated knockdown of such factors, changes of AR-binding sites in prostate cancer cells were analyzed. ChIP-sequence analysis of AR and its associated factors in prostate cancer cells

2014-11-14 | E-GEOD-58428 | biostudies-arrayexpress

TMPRSS2-ERG, HDACs and EZH2 are involved in an AR centric transcriptional circuitry that calibrates androgenic response for prostate cancer progression (gene expression after ERG KD)

Project description: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. Gene expression profiling of human prostate cancer VCaP cells with time course DHT stimulation using microarray.

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TMPRSS2-ERG, HDACs and EZH2 are involved in an AR-centric transcriptional circuitry that calibrates androgenic response for prostate cancer progression

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TMPRSS2-ERG, HDACs and EZH2 are involved in an AR-centric transcriptional circuitry that calibrates androgenic response for prostate cancer progression (gene expression data)

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Genome-wide mapping of retinoblastoma (Rb) binding sites in prostate cancer cell lines VCaP and LNCaP

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TMPRSS2-ERG, HDACs and EZH2 are involved in an AR-centric transcriptional circuitry that calibrates androgenic response for prostate cancer progression (ChIP-Seq data)

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