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Homo sapiens

ABSTRACT: Next Generation Sequencing Facilitates Quantitative Analysis of effect of knockdown of GATA2 on AR binding sites

PROVIDER: PRJNA229904 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1038380.fastq.gz	Fastqsanger.gz
	SRR1038381.fastq.gz	Fastqsanger.gz
	SRR1038382.fastq.gz	Fastqsanger.gz
	SRR1038377.fastq.gz	Fastqsanger.gz
	SRR1038378.fastq.gz	Fastqsanger.gz

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Next Generation Sequencing Facilitates Quantitative Analysis of effect of knockdown of GATA2 on AR binding sites

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare AR binding activity in LNCaP cells with and without knockdown of GATA2. Methods: LNCaP cells between passage number 32-34 were used for assay. Cells are transfected with GATA2 specific or nonspecific siRNA and ChIP was performed, the ChIP producted was further used to generate library with illumina ChIP-seq kit. Hi-seq 2500 was used for sequencing and the data was analyzed by MACs for peaks. Results: GATA2 knockdown lead to changes of AR binding activity , in most AR binding sites, AR shows decreased bindig activity. Only small percent sites show increased binding. Conclusions: Our study represents the first detailed analysis of the relationship between GATA2 and AR binding in whole genomic DNA.These results demostrate GATA2 play a critical role in AR activity in prostate cancer. LNCaP cells was used as cell model were treated with specific GATA2 siRNA.Library was sequenced using Illumina HI-seq 2500.

2014-01-21 | E-GEOD-52725 | biostudies-arrayexpress

Next Generation Sequencing Facilitates Quantitative Analysis of effect of knockdown of GATA2 on AR binding sites

2014-01-21 | GSE52725 | GEO

Pioneer factor FOXA1 defines GATA2- and AR-mediated transcriptional program in prostate cancer [ChIP-Seq]

Project description:AR is tightly regulated by many transcriptional cofactors, including key pioneer factor such as FOXA1 and GATA2. While FOXA1 was recently shown to be able to redistribute AR across the genome, how GATA2 regulates AR cistrome has not been carefully investigated. Here, we report that, unlike FOXA1, GATA2 is unable to reprogram AR, but instead it enhances AR program by inducing AR expression and augmenting AR co-occupancy, thereby acting as a pure AR coactivator, rather than a pioneer factor. On the other hand, AR co-occupancy enhances both GATA2 and FOXA1 binding on the chromatin, forming a positive feedback loop. Importantly, we found that FOXA1 is also capable of reprogramming GATA2 by recruiting GATA2 from GATA motif to FKHD-containing regions, being analogous to its pioneering effect on AR signaling. By contrast, GATA2 simply acts as a co-activator of FOXA1 with a lack of pioneering ability. ChIP_Seq examination of AR, FoxA1 and GATA2 binding sites in LNCaP and DU145 cells

2016-01-11 | E-GEOD-69043 | biostudies-arrayexpress

Homo sapiens

Project description:Next generation sequencing facilitates quantitative analysis of GATA2 binding profile in LNCaP cells.

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Pioneer factor FOXA1 defines GATA2- and AR-mediated transcriptional program in prostate cancer [gene expression]

2016-01-11 | E-GEOD-69044 | biostudies-arrayexpress

Genome-scale CRISPR screens identify PTGES3 as a direct modulator of AR function in advanced prostate cancer

Project description:The androgen receptor (AR) is a critical driver of prostate cancer (PCa). To study regulators of AR protein levels and oncogenic activity, we created the first live cell quantitative endogenous AR fluorescent reporters. Leveraging this novel AR reporter, we performed genome-scale CRISPRi flow cytometry sorting screens to systematically identify genes that modulate AR protein levels. We identified and validated known AR protein regulators including HOXB13 and GATA2 and also unexpected top hits including PTGES3, a poorly characterized gene in PCa. PTGES3 repression resulted in loss of AR protein, cell cycle arrest, and cell death in AR-driven PCa models. PTGES3 is not a commonly essential gene, and our data nominate it as a prime PCa drug target. Clinically, analysis of PCa data demonstrate that PTGES3 expression is associated with AR directed therapy resistance. Mechanistically, we show PTGES3 binds directly to AR, forms a protein complex with AR in the nucleus, regulates AR protein stability in vitro and in vivo and modulates AR function in the nucleus at AR target genes. Lastly using a disulfide tethering fragment screen, we developed a PTGES3 covalent inhibitor that blocks the PTGES3/AR interaction and represses AR signaling in PCa cells, suggesting PTGES3 inhibitors may be a next generation AR-targeting therapeutic strategy that can overcome known mechanisms of resistance to existing AR-directed therapies in PCa.

2025-08-08 | PXD066297 | Pride

Pioneer factor FOXA1 defines GATA2- and AR-mediated transcriptional program in prostate cancer [ChIP-Seq]

2016-01-11 | GSE69043 | GEO

Pioneer factor FOXA1 defines GATA2- and AR-mediated transcriptional program in prostate cancer [gene expression]

2016-01-11 | GSE69044 | GEO

Next Generation Sequencing Facilitates Transcriptomes Quantitative Analysis of siRNA mediated ASGR1 knockdown

Project description:Next Generation Sequencing Facilitates Transcriptomes Quantitative Analysis of siRNA mediated ASGR1 knockdown

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