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Dynamic patterns of DNA methylation in the normal prostate epithelial differentiation program are targets of aberrant methylation in prostate cancer [Methyl Capture]

ABSTRACT: Dynamic patterns of DNA methylation in the normal prostate epithelial differentiation program are targets of aberrant methylation in prostate cancer [Methyl Capture]

PROVIDER: PRJNA730913 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14580503_1.fastq.gz	Fastqsanger.gz
	SRR14580503_2.fastq.gz	Fastqsanger.gz
	SRR14580504_1.fastq.gz	Fastqsanger.gz
	SRR14580504_2.fastq.gz	Fastqsanger.gz
	SRR14580505_1.fastq.gz	Fastqsanger.gz

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Dynamic patterns of DNA methylation in the normal prostate epithelial differentiation program are targets of aberrant methylation in prostate cancer [Methyl Capture]

Project description:Understanding the epigenetic control of normal differentiation programs might yield principal information about critical regulatory states that are disturbed in cancer. We utilized the established non-malignant HPr1-AR prostate epithelial cell model that upon androgen exposure commits to a luminal cell differentiation trajectory from that of a basal-like state. We profile the dynamic transcriptome associated with this transition at multiple time points (0hr, 1hr, 24hr, 96hr), and confirm that expression patterns are strongly indicative of a progressive basal to luminal cell differentiation program based on human expression signatures. Furthermore, we establish dynamic patterns of DNA methylation associated with this program by use of whole genome bisulfite sequencing (WGBS).

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Patterns of aberrant DNA methylation after toxicant-induced malignant transformation (MeDIP-chip dataset 2)

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Dynamic patterns of DNA methylation in the normal prostate epithelial differentiation program are targets of aberrant methylation in prostate cancer

Project description:Dynamic patterns of DNA methylation in the normal prostate epithelial differentiation program are targets of aberrant methylation in prostate cancer

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Patterns of aberrant DNA methylation after toxicant-induced malignant transformation (MeDIP-chip dataset 1)

Project description:Aberrant DNA methylation is frequently observed in cancer. The aim of this study was to determine how DNA methylation is changed after toxicant-induced malignant transformation. This study also puts the DNA methylation changes into context with respect to the aberrant DNA methylation events that occur in bladder and prostate carcinogenesis not associated with toxicant exposure. Immortalized UROtsa (n=3) and RWPE-1 (n=2) are compared to normal HUC (n=2) and PrEC (n=2), respectively. Arsenite (n=1), monomethylarsonous acid (n=2) or cadmium (n=1) transformed UROtsa are compared to parental UROtsa (n=3). Arsenite (n=2), cadmium (n=1) or MNU (n=1) transformed RWPE-1 cells are compared to parental RWPE-1 cells (n=2). Clinical bladder tumor biopsies (n=6), urothelial carcinoma cell lines (n=2) and prostate cancer cell lines (n=3) are compared to thier normal tissue counterparts HUC (n=2) and PrEC (n=2). Immunoprecipitation using anti-methylcytosine (5MeC) antibody.

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Patterns of aberrant DNA methylation after toxicant-induced malignant transformation

Project description:This SuperSeries is composed of the following subset Series: GSE38926: Patterns of aberrant DNA methylation after toxicant-induced malignant transformation (MeDIP-chip dataset 1) GSE38928: Patterns of aberrant DNA methylation after toxicant-induced malignant transformation (MeDIP-chip dataset 2) GSE38929: Patterns of aberrant DNA methylation after toxicant-induced malignant transformation (miRNA dataset) Refer to individual Series

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Dynamic patterns of DNA methylation in the normal prostate epithelial differentiation program are targets of aberrant methylation in prostate cancer [BiSulfite-seq]

Project description:Dynamic patterns of DNA methylation in the normal prostate epithelial differentiation program are targets of aberrant methylation in prostate cancer [BiSulfite-seq]

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Project description:To date, prostate cancer (PCa) remains the most frequently diagnosed cancer in men. While some genetic mutations have been correlated with prostate tumorigenesis, many PCa presentations do not harbor a clear genetic mutation driver. In many cancers, including PCa, aberrant alterations in DNA methylation patterns has been correlated with cancer promotion and progression. The ZBTB methyl-CpG binding proteins (MBPs), consisting of ZBTB33 (Kaiso), ZBTB4 and ZBTB38, constitute a family of transcription factors that selectively recognize mCpG-containing sites. Upon DNA recognition, these MBPs recruit enzyme complexes that act to remodel chromatin and alter transcriptional outcomes. Given the role of these proteins in eliciting epigenetic-based transcription, we sought to comparably analyze protein levels and cellular distribution patterns for all three ZBTB MBPs within 123 cases of prostate adenocarcinomas exhibiting variable Gleason scores. It was generally observed that relative to benign, nuclear and/or cytoplasmic levels of all three ZBTB MBPs increased in prostate tumors, though the expression and predominant localization trends varied between family members and Gleason score. These tumor observations were generally recapitulated in multiple PCa cell line models, prompting comparative analysis of phenotypic and transcriptome alterations after systematic depletion of each ZBTB MBP. While functional overlap between family members was evident, each ZBTB MBP was also found to modulate distinct disease relevant transcription, including at gene targets known to be hyper-methylated in PCa tumors. Collectively, these findings represent the first comparative analysis of all three ZBTB MBP family members within the same disease context and suggest these proteins may be epigenetic-drivers of aberrant transcription in PCa.

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Project description:Beginning with precursor lesions, aberrant DNA methylation marks the entire spectrum of prostate cancer progression. We mapped the global DNA methylation patterns in selected prostate tissues and cell lines using Methylplex-Next Generation Sequencing (M-NGS). Hidden Markov Model based next generation sequence analysis identified ~68,000 methylated regions per sample. While global CpG Island (CGI) methylation was not differential between benign adjacent and cancer samples, overall promoter CGI methylation increased from ~12.6% in benign samples to 19.3% and 21.8% in localized and metastatic cancer tissues, respectively. We found distinct patterns of promoter methylation around transcription start sites, where methylation occurred not only on the CGIs, but also on flanking regions and CGI sparse promoters. Among the 6,691 methylated promoters in prostate tissues, 2481 differentially methylated regions (DMRs) are cancer specific, including numerous novel DMRs. A novel cancer specific DMR in WFDC2 promoter showed heavy methylation in cancer (17/22 tissues, 6/6 cell lines), but not in the benign tissues (0/10) and normal PrEC cells. Integration of LNCaP DNA methylation and H3K4me3 data suggested an epigenetic mechanism for alternate transcription start site utilization and these modifications segregated into distinct regions when present on the same promoter. Finally, we observed differences in repeat element methylation, particularly LINE-1, between ERG gene fusion positive and negative cancers. This comprehensive methylome map will further our understanding of epigenetic regulation in prostate cancer progression. This SuperSeries is composed of the SubSeries listed below.

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