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

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

PROVIDER: PRJNA442593 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6281501.fastq.gz	Fastqsanger.gz
	SRR6281502.fastq.gz	Fastqsanger.gz
	SRR6281503.fastq.gz	Fastqsanger.gz
	SRR6281504.fastq.gz	Fastqsanger.gz
	SRR6873030.fastq.gz	Fastqsanger.gz

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

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

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Functional Significance of Prostate Cancer risk-SNPs

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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.

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Breast cancer risk-associated SNPs modulate the affinity of chromatin for FOXA1 and alter gene expression

Project description:Genome-wide association studies (GWASs) have identified thousands of single nucleotide polymorphisms (SNPs) associated with human traits and diseases. But because the vast majority of these SNPs are located in the noncoding regions of the genome their risk promoting mechanisms are elusive. Employing a new methodology combining cistromics, epigenomics and genotype imputation we annotate the noncoding regions of the genome in breast cancer cells and systematically identify the functional nature of SNPs associated with breast cancer risk. Our results demonstrate that breast cancer risk-associated SNPs are enriched in the cistromes of FOXA1 and ESR1 and the epigenome of H3K4me1 in a cancer and cell-type-specific manner. Furthermore, the majority of these risk-associated SNPs modulate the affinity of chromatin for FOXA1 at distal regulatory elements, which results in allele-specific gene expression, exemplified by the effect of the rs4784227 SNP on the TOX3 gene found within the 16q12.1 risk locus. Examination of histone modification H3K4me2 in untreated and E2 treated cells

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