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N6-methyladenine DNA Modification in Glioblastoma [ChIP-seq, BiSulfite-seq, DIP-seq]

ABSTRACT: N6-methyladenine DNA Modification in Glioblastoma [ChIP-seq, BiSulfite-seq, DIP-seq]

PROVIDER: PRJNA488098 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7759680_1.fastq.gz	Fastqsanger.gz
	SRR7759680_2.fastq.gz	Fastqsanger.gz
	SRR7759690_1.fastq.gz	Fastqsanger.gz
	SRR7759690_2.fastq.gz	Fastqsanger.gz
	SRR7759700_1.fastq.gz	Fastqsanger.gz

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N6-methyladenine DNA Modification in Glioblastoma [ChIP-seq, BiSulfite-seq, DIP-seq]

Project description:Genetic drivers of cancer can be dysregulated through epigenetic modifications of DNA. While the critical role of DNA 5-methylcytosine (5mC) in the regulation of transcription is recognized, the functions of other non-canonical DNA modifications remain obsure. Here, we report the identification of novel N(6)-methyladenine (N6-mA) DNA modifications in human tissues and implicate this epigenetic regulation in human disease, the highly malignant brain cancer, glioblastoma. Glioblastoma upregulates N6-mA levels, which co-localize with heterochromatic histone modifications, namely H3K9me3. N6-mA levels are dynamically regulated by the DNA demethylase, ALKBH1, to transcriptionally silence oncogenic pathways through decreasing chromatin accessibility. Targeting the N6-mA regulator, ALKBH1, in patient-derived human glioblastoma models inhibited tumor cell proliferation and extended survival of tumor-bearing mice, supporting this novel DNA modification as a potential new molecular therapeutic target for glioblastoma. Collectively, our results uncover a novel epigenetic node in cancer through the DNA modification, N6-mA.

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N6-methyladenine DNA Modification in Glioblastoma [RNA-seq]

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N6-methyladenine DNA Modification in Glioblastoma [ATAC-seq]

Project description:N6-methyladenine DNA Modification in Glioblastoma [ATAC-seq]

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N6-Methyladenine DNA Modification in Human Genome

Project description:In human cells, 5-methylcytosine (5mC) DNA modification plays an important role in gene regulation. However, N6-methyladenine (6mA) DNA modification, which is predominantly present in prokaryotes, is considered to be absent in human genomic DNA. Here, using single molecule real-time (SMRT) sequencing on human blood, we show that DNA 6mA modification is extensively present in human genome, accounting for ~0.051% of the total adenines. [G/C]AGG[C/T] was the most significant motif associated with 6mA modification. 6mA sites are enriched in the exon coding regions and are associated with transcriptional activation. DNA N6-methyladenine and N6-demethyladenine modification in human are mediated by methyltransferase N6AMT1 and demethylase ALKBH1, respectively. The 6mA abundance is significantly lower in cancer tissues compared to adjacent normal tissues, which is accompanied with decreased N6AMT1 and increased ALKBH1 levels. Decrease of 6mA modification level stimulated tumorigenesis in human. Collectively, our results demonstrate that 6mA DNA modification is present in human tissues, and we describe a potential role of the N6AMT1/ALKBH1-6mA regulatory axis in the progression of human cancer.

2017-10-02 | GSE104475 | GEO

N6-methyladenine DNA Modification in Glioblastoma [RNA-seq]

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N6-methyladenine DNA Modification in Glioblastoma [ATAC-seq]

Project description:Genetic drivers of cancer can be dysregulated through epigenetic modifications of DNA. While the critical role of DNA 5-methylcytosine (5mC) in the regulation of transcription is recognized, the functions of other non-canonical DNA modifications remain obscure. Here, we report the identification of novel N(6)-methyladenine (N6-mA) DNA modifications in human tissues and implicate this epigenetic regulation in human disease, the highly malignant brain cancer, glioblastoma. Glioblastoma upregulates N6-mA levels, which co-localize with heterochromatic histone modifications, namely H3K9me3. N6-mA levels are dynamically regulated by the DNA demethylase, ALKBH1, to transcriptionally silence oncogenic pathways through decreasing chromatin accessibility. Targeting the N6-mA regulator, ALKBH1, in patient-derived human glioblastoma models inhibited tumor cell proliferation and extended survival of tumor-bearing mice, supporting this novel DNA modification as a potential new molecular therapeutic target for glioblastoma. Collectively, our results uncover a novel epigenetic node in cancer through the DNA modification, N6-mA.

2018-11-01 | GSE118092 | GEO

N6-Methyladenine DNA Modification in Human Genome

Project description:N6-Methyladenine DNA Modification in Human Genome

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Identify the interplay between N6-methyladenine and gene regulation under hypoxia by randomized empirical model (RNA-seq)

Project description:In this study, we employed RNA-seq to investigate the role of N6-methyladenine (6mA) in chromatin accessibility under hypoxic conditions.

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Identify the interplay between N6-methyladenine and gene regulation under hypoxia by randomized empirical model (ATAC-seq)

Project description:In this study, we employed ATAC-seq (Assay for Transposase-Accessible Chromatin using sequencing) to investigate the role of N6-methyladenine (6mA) in chromatin accessibility under hypoxic conditions.

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