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Risk SNPs mediated promoter-enhancer switching promotes prostate cancer progression through lncRNA PCAT19 (ChIP-seq data set)

ABSTRACT: Risk SNPs mediated promoter-enhancer switching promotes prostate cancer progression through lncRNA PCAT19 (ChIP-seq data set)

PROVIDER: PRJNA439377 | ENA |

REPOSITORIES: ENA

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Risk SNPs mediated promoter-enhancer switching promotes prostate cancer progression through lncRNA PCAT19

Project description:Risk SNPs mediated promoter-enhancer switching promotes prostate cancer progression through lncRNA PCAT19

| PRJNA442593 | ENA

Risk SNPs mediated promoter-enhancer switching promotes prostate cancer progression through lncRNA PCAT19 (RNA-seq data sets)

Project description:Risk SNPs mediated promoter-enhancer switching promotes prostate cancer progression through lncRNA PCAT19 (RNA-seq data sets)

| PRJNA417969 | ENA

Risk SNPs mediated promoter-enhancer switching promotes prostate cancer progression through lncRNA PCAT19 (ChIP-seq data set)

Project description:To determine the binding of H3K4me1 and H3K4me3 to PCAT19 locus, we performed ChIP-seq in 22Rv1 cells.

2019-03-11 | GSE112120 | GEO

Risk SNPs mediated promoter-enhancer switching promotes prostate cancer progression through lncRNA PCAT19

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-03-11 | GSE112164 | GEO

Risk SNPs mediated promoter-enhancer switching promotes prostate cancer progression through lncRNA PCAT19 (RNA-seq data sets)

Project description:To determine the functional mechanisms of PCAT19-long isoform and HNRNPAB, we conducted siRNA knockdown RNA-sequencing in prostate cancer cell line V16A.

2019-03-11 | GSE106774 | GEO

Prostate Cancer Risk SNPs enriched in Androgen Receptor Binding Sites

Project description:Genome-wide association studies (GWAS) have identified dozens of genomic loci, whose single nucleotide polymorphisms (SNPs) predispose to prostate cancer (PCa). However, the biological functions of these common genetic variants and the mechanisms to increase disease risk are largely unknown. We integrated chromatin-IP coupled sequencing (ChIP-seq) and microarray expression profiling in the TMPRSS2-ERG gene rearrangement positive DuCaP cell model with the NHGRI GWAS PCa risk SNPs catalog, in an attempt to identify disease susceptibility SNPs localized within functional androgen receptor binding sites (ARBSs). Among the 48 GWAS index SNPs and 2,702 linked SNPs defined by the 1000G project 104 were found to be localized in the AR ChIP-seq peaks. Of these risk SNPs, rs11891426 T/G in the 7th intron of its host gene melanophilin (MLPH) was found located within a putative auxiliary ARE motif, which we found enriched in the neighborhood of canonical ARE motifs. Exchange of T to G attenuated the transcriptional activity of the MLPH-ARBS in a reporter gene assay. The expression of MLPH protein in tissue samples from prostate cancer patients was significantly lower in those with the G compared to the T allele. Moreover, a significant positive correlation of AR and MLPH protein expression levels was also confirmed in tissue samples. These results unravel a hidden link between AR and a functional PCa risk SNP rs11891426, whose allele alteration affects androgen regulation of its host gene MLPH. This study shows the power of integrative studies to pin down functional risk SNPs and justifies further investigations.

2015-10-12 | GSE63693 | GEO

Prostate Cancer Risk SNPs in Androgen Receptor Target Sites

Project description:We profiled androgen receptor (AR) genomic targets using high-throughput sequencing of chromatin-immunoprecipitated (ChIP) DNA from TMPRSS2-ERG fusion gene positive DUCaP prostate cancer cells. ChIp-seq and microarray gene expression profiling datasets were integrated with the NHGRI GWAS PCa risk SNPs catalog to identify disease susceptibility SNPs localized within functional androgen receptor binding sites (ARBSs). Eighty GWAS index or linked SNPs were found to be localized in ARBSs. Among these rs11891426:T>G in the 7th intron of the melanophilin gene was found located within a novel putative auxiliary AR binding motif, which we found enriched in the neighborhood of canonical androgen responsive elements. T→G exchange attenuated the transcriptional activity of the ARBS in an AR reporter gene assay of prostate cancer cell models. It went also in line with decreased melanophilin protein level in primary prostate tumors with G allele.These results unravel a hidden link between androgen receptor and a functional PCa risk SNP, whose allele alteration affects androgen regulation of its host gene melanophilin . Genomic profile of androgen receptor binding sites of androgen or vehicle treated DUCaP cells using ChIP-seq. IgG precipiated DNAs from both treatments served as controls.

2015-07-10 | E-GEOD-70679 | biostudies-arrayexpress

Prostate Cancer Risk SNPs in Androgen Receptor Target Sites

2015-07-10 | GSE70679 | GEO

Functional Significance of Prostate Cancer risk-SNPs

Project description:Functional Significance of Prostate Cancer risk-SNPs

| PRJNA294704 | ENA

Systematic identification of human SNPs affecting regulatory element activity

Project description:Most of the millions of single-nucleotide polymorphisms (SNPs) in the human genome are non-coding, and many overlap with putative regulatory elements. Genome-wide association studies have linked many of these SNPs to human traits or to gene expression levels, but rarely with sufficient resolution to identify the causal SNPs. Functional screens based on reporter assays have previously been of insufficient throughput to test the vast space of SNPs for possible effects on enhancer and promoter activity. Here, we have leveraged the throughput of the SuRE reporter technology to survey a total of 5.9 million SNPs, including 57% of the known common SNPs world-wide. We identified more than 30 thousand SNPs that alter the activity of putative regulatory elements, often in a cell-type specific manner. These data indicate that a large proportion of human non-coding SNPs may affect gene regulation. Integration of these SuRE data with genome-wide association studies may help to identify causal SNPs.

2019-04-05 | GSE128325 | GEO

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