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Dnmt3a associates with promoters and enhancers to protect epidermal stem cells from cancer [MeDIP-seq]

ABSTRACT: Dnmt3a associates with promoters and enhancers to protect epidermal stem cells from cancer [MeDIP-seq]

PROVIDER: PRJNA615674 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11430462.fastq.gz	Fastqsanger.gz
	SRR11430463.fastq.gz	Fastqsanger.gz
	SRR11430464.fastq.gz	Fastqsanger.gz
	SRR11430465.fastq.gz	Fastqsanger.gz
	SRR11430466.fastq.gz	Fastqsanger.gz

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Similar Datasets

Dnmt3a associates with promoters and enhancers to protect epidermal stem cells from cancer [MeDIP-seq]

Project description:The de novo DNA methyltransferase Dnmt3a is mutated in human acute myeloid leukemia, and suppresses tumorigenesis in murine models of leukemia and lung cancer. Conversely, deregulation of the other de novo DNA methyltransferase, Dnmt3b, predominantly promotes tumorigenesis. However, the molecular mechanisms underlying the roles of Dnmt3a and Dnmt3b in cancer remain poorly understood. Using conditional knockout mice, here we show that Dnmt3a -- but not Dnmt3b -- strongly protects epidermal stem cells from carcinogen-induced tumor initiation, without affecting the progression of benign lesions to aggressive carcinomas. Only upon combined deletion of Dnmt3a and Dnmt3b, squamous cell carcinomas acquired a more aggressive fate and even became metastatic, indicating that Dnmt3b is tumor-suppressive, rather than pro-tumorigenic, in epidermal neoplasia. Mechanistically, Dnmt3a promotes the expression of epidermal differentiation genes by interacting with their enhancers, and inhibits the expression of lipid metabolism and cell proliferation genes by directly methylating their promoters. Altogether, we demonstrate that Dnmt3a, but not Dnmt3b, is critical for suppressing epidermal tumor initiation, while both enzymes prevent tumor progression.

2020-03-26 | GSE92422 | GEO

Dnmt3a associates with promoters and enhancers to protect epidermal stem cells from cancer [RNA-seq]

Project description:Dnmt3a associates with promoters and enhancers to protect epidermal stem cells from cancer [RNA-seq]

| PRJNA623588 | ENA

Dnmt3a associates with promoters and enhancers to protect epidermal stem cells from cancer [ChIP-seq]

2017-06-13 | GSE92421 | GEO

Dnmt3a associates with promoters and enhancers to protect epidermal stem cells from cancer [RNA-seq]

2020-04-07 | GSE92423 | GEO

DNA methylation of dnmt3a deficient Kras lung tumors and dnmt3a wt Kras lung tumors

Project description:To examine whether Dnmt3a deficiency resulted in genomic methylation changes we performed an unbiased methylome analysis. Methylated DNA isolated from three Dnmt3a deficient and two WT tumors was immunoprecipitated and subjected to high throughput sequencing (MeDIP-Seq). We observed that genes that were less expressed in Dnmt3a deficient tumors tended to have lower methylation levels in gene bodies. Examination of methylcytosine in two tumor types

2011-10-25 | E-GEOD-32484 | biostudies-arrayexpress

DNA methylation of dnmt3a deficient Kras lung tumors and dnmt3a wt Kras lung tumors

2011-10-26 | GSE32484 | GEO

DNMT3A Reads and Connects Histone H3K36me2 to DNA methylation [MeDIP-Seq]

Project description:DNMT3A Reads and Connects Histone H3K36me2 to DNA methylation [MeDIP-Seq]

| PRJNA589274 | ENA

Abnormal RNA splicing and genomic instability after induction of DNMT3A mutations by CRISPR/Cas9 gene editing [MeDIP-Seq]

Project description:Purpose: DNA methyltransferase 3A (DNMT3A) mediates de novo DNA methylation. Mutations in DNMT3A are associated with hematological malignancies, most frequently acute myeloid leukemia. DNMT3A mutations are hypothesized to establish a pre-leukemic state, rendering cells vulnerable to secondary oncogenic mutations and malignant transformation. However, the mechanisms by which DNMT3A mutations contribute to leukemogenesis are not well-defined. Methods: Methylated DNA immunoprecipitation (MeDIP) was used to detect regional differences in DNA methylation between DNMT3A WT and MT clones. DNA extraction of WTblk, WT1, MT1, MT2, and MT4 cell lines was performed as previously described. 5-mC profiling, fragmentation, library preparation and sequencing were performed by Otogenetics (Atlanta, GA, USA). In brief, paired-end libraries were generated using the Illumina TruSeq DNA sample preparation kit. Illumina HiSeq2500 was used for sequencing with a paired-end sequencing length of 100-125 bp and approximately 40 million reads per sample. Results: We attempted to identify differentially methylated genes based on DNMT3A mutation status and found very few regions of differential methylation between WT and MT cell lines (Figure 3C), which did not exceed the number of regions expected to exhibit differential methylation by chance alone. These data suggest that regional methylation patterns do not differ between DNMT3A MT and WT cell lines in our gene-edited K562 cells. Conclusions: CRISPR/Cas9-mediated DNMT3A-mutated K562 cells may be used to model effects of DNMT3A mutations in human cells. Our findings implicate aberrant splicing and induction of genomic instability as potential mechanisms by which DNMT3A mutations might predispose to malignancy.

2018-01-09 | GSE96577 | GEO

MeDIP-chip from clinical cervical tissues in promoters

Project description:Utilizing methylation DNA immunoprecipitation (MeDIP) coupled with promoter tiling arrays, we analyzed the methylation profiles of pooled DNA from human cervical carcinoma and normal cervix

2012-08-06 | GSE33187 | GEO

DNMT3A Reads and Connects Histone H3K36me2 to DNA methylation [MeDIP-Seq]

Project description:DNA methylation at the 5-position of cytosine (5mC) is a crucial epigenetic mark in regulating biological processes including gene silencing, gene imprinting, and X chromosome inactivation. It has long been questioned how de novo DNA 5mC patterns are established in different genomic regions and whether histone modifications crosstalk to the process. Here, we report a previously uncovered mechanism of histone mark H3K36me2 in recruiting and activating DNMT3A, primarily in the intergenic regions. Our biochemistry studies discovered that H3K36me2 could be specifically bound by DNMT3A PWWP domain and substantially stimulate DNMT3A activity, representing the first example of histone modification in activating DNMT3A activity. Using multiple myeloma model, KMS11, we further found that the genome-wide gain-of-H3K36me2 resulted in global increase of 5mC, primarily in the intergenic regions. Importantly, DNA inhibitor treatment specifically blocked KMS11 growth demonstrating the functional importance of this regulatory pathway.

2019-12-31 | GSE140303 | GEO

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