Genomewide nucleosome occupancy and DNA methylation analysis on normal and prostate cancer cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE94361 | GEO | 2017/02/01
SECONDARY ACCESSION(S): PRJNA369473
REPOSITORIES: GEO
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Project description:Near promoters, both nucleosomes and CpG sites form characteristic spatial patterns. Previously, nucleosome depleted regions were observed upstream of transcription start sites and nucleosome occupancy was reported to correlate both with CpG density and the level of CpG methylation. Several studies imply a causal link where CpG methylation might induce nucleosome formation, whereas others argue the opposite, i.e., that nucleosome occupancy might influence CpG methylation. Correlations are indeed evident between nucleosomes, CpG density and CpG methylation-at least near promoter sites. It is however less established whether there is an immediate causal relation between nucleosome occupancy and the presence of CpG sites-or if nucleosome occupancy could be influenced by other factors. In this work, we test for such causality in human genomes by analyzing the three quantities both near and away from promoter sites. For data from the human genome we compare promoter regions with given CpG densities with genomic regions without promoters but of similar CpG densities. We find the observed correlation between nucleosome occupancy and CpG density, respectively CpG methylation, to be specific to promoter regions. In other regions along the genome nucleosome occupancy is statistically independent of the positioning of CpGs or their methylation levels. Anti-correlation between CpG density and methylation level is however similarly strong in both regions. On promoters, nucleosome occupancy is more strongly affected by the level of gene expression than CpG density or CpG methylation-calling into question any direct causal relation between nucleosome occupancy and CpG organization. Rather, our results suggest that for organisms with cytosine methylation nucleosome occupancy might be primarily linked to gene expression, with no strong impact on methylation.
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Project description:Purpose: Profile global expression of prostatic tumors to compare with published datasets. Methods: Prostate tumors were flash frozen followed by processed for total RNA using the RNeasy kit (Qiagen). Samples were submitted for polyA library preparation and bulk RNA-sequencing. Conclusions: Global gene expression profiling and comparison of prostate tumor genotypes suggests differential enrichment of neuroendocrine signatures that match established human neuroendocrine prostate cancer expression signatures.
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Project description:The stromal microenvironment plays key roles in prostate development and cancer. Cancer associated fibroblasts (CAFs) and other stromal cells stimulate tumourigenesis via several mechanisms including the expression of pro-tumourigenic factors. Mesenchyme (embryonic stroma) controls prostate organogenesis, and in some circumstances can re-differentiate prostate tumours. Epithelia are regulated by powerful paracrine signalling from the stroma in both development and disease, and identification of these stromal signals is important. We have applied next-generation Tag profiling to fetal human prostate, normal human prostate fibroblasts (NPFs) and CAFs to identify molecules expressed in prostatic stroma
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Project description:MNase-Seq for nucleosome occupancy
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Project description:The stromal microenvironment plays key roles in prostate development and cancer. Cancer associated fibroblasts (CAFs) and other stromal cells stimulate tumourigenesis via several mechanisms including the expression of pro-tumourigenic factors. Mesenchyme (embryonic stroma) controls prostate organogenesis, and in some circumstances can re-differentiate prostate tumours. Epithelia are regulated by powerful paracrine signalling from the stroma in both development and disease, and identification of these stromal signals is important. We have applied next-generation Tag profiling to fetal human prostate, normal human prostate fibroblasts (NPFs) and CAFs to identify molecules expressed in prostatic stroma Each sample was used for Tag library construction, by Solexa Inc
2011-10-22 | E-GEOD-25018 | biostudies-arrayexpress
Project description:To identify prostate cancer-specific gene expression, we have employed whole cDNA microarray expression profiling between benign prostate hypertrophy and prostate cancer. We performed needle biopsy of patients with prostatic hyperplasia who were suspected as prostate cancer for minor high level (4.0-10 ng/ml). As a result of needle biopsy, we used the tissue of patients with prostatic hyperplasia that prostate cancer was denied for cDNA microarry analysis. Furthermore, we also performed needle biopsy of patients that prostate cancer should have been strongly suspected because of high PSA. Needle biopsies were performed after we obtained informed consent from patients with the document approved from the Graduate School of Medical Science, Kanazawa University. Gene expression profile was determied in each of normal prostate samples and prostate cancer samples. Then the profiles were compared between normal prostate samples and prostate cancer samples.
2014-07-30 | E-GEOD-30994 | biostudies-arrayexpress
Project description:To identify prostate cancer-specific gene expression, we have employed whole cDNA microarray expression profiling between benign prostate hypertrophy and prostate cancer. We performed needle biopsy of patients with prostatic hyperplasia who were suspected as prostate cancer for minor high level (4.0-10 ng/ml). As a result of needle biopsy, we used the tissue of patients with prostatic hyperplasia that prostate cancer was denied for cDNA microarry analysis. Furthermore, we also performed needle biopsy of patients that prostate cancer should have been strongly suspected because of high PSA. Needle biopsies were performed after we obtained informed consent from patients with the document approved from the Graduate School of Medical Science, Kanazawa University.
2014-07-30 | GSE30994 | GEO
Project description:BackgroundDNA methylation is an epigenetic modification that is enriched in heterochromatin but depleted at active promoters and enhancers. However, the debate on whether or not DNA methylation is a reliable indicator of high nucleosome occupancy has not been settled. For example, the methylation levels of DNA flanking CTCF sites are higher in linker DNA than in nucleosomal DNA, while other studies have shown that the nucleosome core is the preferred site of methylation. In this study, we make progress toward understanding these conflicting phenomena by implementing a bioinformatics approach that combines MNase-seq and NOMe-seq data and by comprehensively profiling DNA methylation and nucleosome occupancy throughout the human genome.ResultsThe results demonstrated that increasing methylated CpG density is correlated with nucleosome occupancy in the total genome and within nearly all subgenomic regions. Features with elevated methylated CpG density such as exons, SINE-Alu sequences, H3K36-trimethylated peaks, and methylated CpG islands are among the highest nucleosome occupied elements in the genome, while some of the lowest occupancies are displayed by unmethylated CpG islands and unmethylated transcription factor binding sites. Additionally, outside of CpG islands, the density of CpGs within nucleosomes was shown to be important for the nucleosomal location of DNA methylation with low CpG frequencies favoring linker methylation and high CpG frequencies favoring core particle methylation. Prominent exceptions to the correlations between methylated CpG density and nucleosome occupancy include CpG islands marked by H3K27me3 and CpG-poor heterochromatin marked by H3K9me3, and these modifications, along with DNA methylation, distinguish the major silencing mechanisms of the human epigenome.ConclusionsThus, the relationship between DNA methylation and nucleosome occupancy is influenced by the density of methylated CpG dinucleotides and by other epigenomic components in chromatin.
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