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Differential expression profiling of the TamR cells following AR knockdown

ABSTRACT: Differential expression profiling of the TamR cells following AR knockdown

PROVIDER: PRJNA474440 | ENA |

REPOSITORIES: ENA

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Differential expression profiling of the TamR cells following AR knockdown

Project description:The androgen receptor (AR) has emerged as a candidate target for the treatment of breast cancer. In this study, we sought to characterize the functional consequences of AR knockdown using a siRNA-mediated approach in a tamoxifen-resistant (TamR) derivative of MCF7 breast cancer cell line.

2018-06-05 | GSE115270 | GEO

Genome-wide expression profiling of Hic-5 knockdown in PshTert-AR human myofibroblasts

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Genome-wide expression profiling of Hic-5 knockdown in PshTert-AR human myofibroblasts

Project description:Identifying the effect of the co-regulator Hic-5 (TGFB1I1) on global androgen receptor transcriptional activity in PShTert-AR prostate fibroblast cells with view to further elucidating the broader biological role of Hic-5 on fibroblast spceific androgen signaling. Knockdown of Hic5 for 48 hours in PShTert-AR cells significantly altered the androgen regulation of approximately 1347 genes. The effect of Hic-5 knockdown was to suppress androgen regulation of approximately 85% of those transcripts, by either reducing androgen mediated repression or activition of gene expression. PShTert-AR cells were transfected with 10nM non-specific control siRNA (NS) or with commercially avaliable Hic-5 specific siRNA (siHic5) for 24hrs. Cells were kept in 5% hormone stripped FBS RPMI for a further 24 hours and subsequently treated with either ethanol vehicle control or 10nM DHT for 16hr. Total RNA was extracted. Nine independent vehicle and 9 DHT siNS and siHic5 samples were pooled into three groups of vechicle and DHT treated siNS and siHic5 samples and hybrydised to Affymetrix Human Gene 1.0 ST array chips.

2013-08-26 | E-GEOD-47203 | biostudies-arrayexpress

Gene Expression in Castration-Resistant C4-2 Cells after AR Knockdown

Project description:Prostate cancer is the most common, lethal malignancy in men. Although androgen withdrawal therapies are used to treat advanced disease, progression to a castration-resistant, end-stage is the usual outcome. In this study, the tested hypothesis was that the androgen receptor remains essential for the growth and viability of castration-resistant disease. Knocking down the androgen receptor in well-established tumors grown in castrated mice caused growth arrest, decreased serum PSA, and frequently regression and total eradication of tumors. Growth control of castration-resistant tumors appeared to be linked to the extent of androgen receptor knockdown, which triggers upregulation of many genes involved in apoptosis, cell cycle arrest, and inhibition of tumorigenesis and protein synthesis. Our findings provide proof of principle that in vivo knockdown of the androgen receptor is a viable therapeutic strategy to control and possibly eradicate prostate cancers that have progressed to the lethal castration-resistant state. C4-2 human prostate cancer cells stably expressing a tetracycline-inducible AR-targeted short hairpin RNA (shRNA) or scrambled shRNA were generated. These two cell lines were incubated in the absence of androgens with or without doxycycline hyclase (DOX). Comparison analysis of the gene expression profiles of C4-2 cells stably expressing AR shRNA + DOX and control cells (AR shRNA - DOX and scrambled shRNA Â± DOX) was conducted to identify differentially regulated genes due to AR knockdown after normalization and data filtering. Genes were considered to be significantly different if the expression in the induced AR shRNA + DOX cells was at least 1.7-fold greater or 1.7-fold less than that seen in the control cells, with P< 0.05.

2010-06-23 | E-GEOD-13332 | biostudies-arrayexpress

Transcriptional profiling following knockdown of RNA binding proteins

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Transcriptome profiling following knockdown of NAA50 in Arabidopsis

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Gene expression profiling data following TRIM8 knockdown in MCF-7 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.

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