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Homo sapiens

ABSTRACT: Effect of ETV1 knockdown on genome wide AR binding in LNCaP Cells

PROVIDER: PRJNA203679 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR863535.fastq.gz	Fastqsanger.gz
	SRR863536.fastq.gz	Fastqsanger.gz
	SRR863537.fastq.gz	Fastqsanger.gz
	SRR863538.fastq.gz	Fastqsanger.gz
	SRR863539.fastq.gz	Fastqsanger.gz

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Effect of ETV1 knockdown on genome wide AR binding in LNCaP Cells

Project description:Translocation of ETS transcription factors including ERG and ETV1 occur in half of all prostate cancers. LNCaP cells harbor an ETV1 translocation. We performed ChIP-Seq analysis to determine the role of ETV1 on AR binding. The localization of enhancers were determined by H3K4me1 ChIP-Seq. To determine ETV1 and H3K4me1 localization, logarithmically growing cells

2013-06-13 | E-GEOD-47120 | biostudies-arrayexpress

Effect of ETV1 knockdown on genome wide AR binding in LNCaP Cells

2013-06-13 | GSE47120 | GEO

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Project description:Gene expression profile of ETV1 knockdown in LNCaP prostate cancer cells

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Project description:Transcriptional effect of ETV1 knockdown in melanoma cells

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Effects of Cardiac Glycosides on RNA Expression in Prostate Cancer LNCaP-abl Cells

Project description:Prostate cancer is the most common cancer in men and cardiac glycosides inhibit prostate cancer cell proliferation. In order to investigate the mechanism by which cardiac glycosides inhibit prostate cancer cells, we observed genome-wide RNA expression in prostate cancer LNCaP-abl cells, hormone resistant cells, after the cardiac glycoside treatment using RNA-Seq. In addition, we profiled LNCaP-abl cells after androgen receptor (AR) knockdown to observe whether cardiac glycoside effect on RNA expression is similar to that of AR knockdown. Observation of three cardioglycosides, Digoxin, Peruvoside and Strophanthidin, and AR knockdown regulated RNA expression in LNCaP-abl with RNA-Seq (each triplicates)

2012-04-03 | E-GEOD-35126 | biostudies-arrayexpress

ChIP-Seq in LNCaP prostate cancer cells

Project description:We used ChIP-Seq to profile AR binding and H3K27 acetylation genome-wide in LNCaP cells with and without PRMT inhibition and knockdown.

2022-01-28 | GSE153661 | GEO

Effect of p53 knowkdown on genome-wide map of AR-DNA binding

Project description:We report that p53 knockdown changed AR-DNA binding across the genome. We found fewer AR-binding sites in the absence of p53. Examination of AR-DNA binding after p53 knockdown in LNCaP cells

2012-07-31 | E-GEOD-31294 | biostudies-arrayexpress

Effects of Cardiac Glycosides on RNA Expression in Prostate Cancer LNCaP-abl Cells

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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

FoxA1 inhibits androgen receptor expression and suppresses prostate cancer metastasis [LNCaP, ChIP-seq]

Project description:FoxA1 has been shown critical for prostate development and prostate-specific gene expression regulation. In addition to its well-established role as an AR pioneering factor,several studies have recently revealed significant AR binding events in prostate cancer cells with FoxA1 knockdown. Furthermore, the role of FoxA1 itself in prostate cancer has not been carefully examined. Thus, it is important to understand the role of FoxA1 in prostate cancer and how it interacts with AR signaling. To address these questions, we generated LNCaP cells with stable FoxA1 knockdown. We performed AR/FoxA1 ChIP-seq and microarray analysis of these cells. ChIP_Seq examination of AR and FoxA1 binding sites in LNCaP shCtrl and shFoxA1 cells

2014-06-02 | E-GEOD-37345 | biostudies-arrayexpress

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