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Altered 5-hydroxymethylcytosine landscape in primary gastric adenocarcinoma

ABSTRACT: Altered 5-hydroxymethylcytosine landscape in primary gastric adenocarcinoma

PROVIDER: PRJNA556817 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9842370.fastq.gz	Fastqsanger.gz
	SRR9842380.fastq.gz	Fastqsanger.gz
	SRR9842371.fastq.gz	Fastqsanger.gz
	SRR9842372.fastq.gz	Fastqsanger.gz
	SRR9842363.fastq.gz	Fastqsanger.gz

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Altered 5-hydroxymethylcytosine landscape in primary gastric adenocarcinoma

Project description:Altered 5-hydroxymethylcytosine landscape in primary gastric adenocarcinoma

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Altered 5-hydroxymethylcytosine landscape in primary gastric adenocarcinoma

Project description:Multiple factors, including molecular, genetic, and epigenetic changes, have been linked to gastric cancer formation and progression. Cytosine methylation (5mC) has been well studied and recognized as a critical epigenetic mark in the mammalian genome. The recent novel discovery of 5-hydroxymethylcytosine (5hmC), which generated by ten-eleven translocation (TET) enzymes, provide new perspective to understand DNA methylation-related plasticity. Here we show that gastric tumors display significant loss of 5hmC. Using matched distant normal, peripheral and tumor primary tissues, we performed genome-wide profiling of 5hmC and identified differentially hydroxymethylated regions (DhMRs) specifically associated with gastric tumors. Gene Ontology (GO) analyses indicated that DhMRs (both loss-of-5hmC and gain-of-5hmC) were enriched among the genes involved in specific pathways. Interestingly the binding motif of hypoxia-inducible factor 1 (HIF1) is enriched among both peripheral and tumor DhMRs, while the Myc-binding motif is specifically enriched among only tumor DhMRs. Tumor progression analyses revealed a unique set of DhMRs that correlate with tumor progression. These data together suggest that the alteration of 5hmC could potentially contribute to the tumorigenesis of gastric tumors.

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Somatic Promoter Landscape of Primary Gastric Adenocarcinoma Delineated by Epigenomic Profiling

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