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The molecular mechanism and clinical significance of IGF2BP3 in adenocarcinoma of the esophagogastric junction [RNA-seq]

ABSTRACT: The molecular mechanism and clinical significance of IGF2BP3 in adenocarcinoma of the esophagogastric junction [RNA-seq]

PROVIDER: PRJNA1085747 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28274949_1.fastq.gz	Fastqsanger.gz
	SRR28274949_2.fastq.gz	Fastqsanger.gz
	SRR28274950_1.fastq.gz	Fastqsanger.gz
	SRR28274950_2.fastq.gz	Fastqsanger.gz
	SRR28274951_1.fastq.gz	Fastqsanger.gz

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The molecular mechanism and clinical significance of IGF2BP3 in adenocarcinoma of the esophagogastric junction [RIP-seq]

Project description:To reveal the potential targets of IGF2BP3 in Adenocarcinoma of the esophagogastric junction, we performed IGF2BP3 Immunoprecipitation sequencing (RIP-seq) in OE-19 cells.

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The molecular mechanism and clinical significance of IGF2BP3 in adenocarcinoma of the esophagogastric junction [RNA-seq]

Project description:To explore the major function of IGF2BP3 in Adenocarcinoma of the esophagogastric junction, we conducted RNA sequencing (RNA-seq) in IGF2BP3 KD OE-19 cells.

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The molecular mechanism and clinical significance of IGF2BP3 in adenocarcinoma of the esophagogastric junction [LACE-seq]

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The molecular mechanism and clinical significance of IGF2BP3 in adenocarcinoma of the esophagogastric junction [meRIP-seq]

Project description:To reveal the potential m6A modification gene in Adenocarcinoma of the esophagogastric junction, we performed methylated RNA immunoprecipitation and sequencing (meRIP-seq) in OE-19 cells.

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The molecular mechanism and clinical significance of IGF2BP3 in adenocarcinoma of the esophagogastric junction [meRIP-seq]

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The molecular mechanism and clinical significance of IGF2BP3 in adenocarcinoma of the esophagogastric junction [RIP-seq]

Project description:The molecular mechanism and clinical significance of IGF2BP3 in adenocarcinoma of the esophagogastric junction [RIP-seq]

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The molecular mechanism and clinical significance of IGF2BP3 in adenocarcinoma of the esophagogastric junction [LACE-seq]

Project description:The molecular mechanism and clinical significance of IGF2BP3 in adenocarcinoma of the esophagogastric junction [LACE-seq]

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m6A full transcriptome map of human adenocarcinoma of esophagogastric junction

Project description:Here we systematically analyze the modification pattern of m6A mRNA in adenocarcinoma at the esophagogastric junction.In adenocarcinoma of esophagogastric junction samples, a total of 4775 new m6A peaks appeared, and 3054 peaks disappeared. The unique m6A-related genes in adenocarcinoma of esophagogastric junction are related to cancer-related pathways. There are hypermethylated or hypomethylated m6A peaks in AEG in differentially expressed mRNA transcripts. This study preliminarily constructed the first m6A full transcriptome map of human adenocarcinoma of esophagogastric junction. This has a guiding role in revealing the mechanism of m6A-mediated gene expression regulation.

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m6A full transcriptome map of human adenocarcinoma of esophagogastric junction

Project description:m6A full transcriptome map of human adenocarcinoma of esophagogastric junction

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Gastric and esophagogastric junction adenocarcinoma with infrequent hypermethylation show poor prognosis

Project description:Background Gastric cancer (GC) was characterized by unique DNA methylation epigenotypes (MEs). Still, MEs, including adenocarcinoma of the esophagogastric junction (AEG) and background non-neoplastic columnar mucosae (NM), are yet to be clarified. Methods We analyzed genome-wide DNA MEs of AEG, GC, and background NM using Infinium 450k beadarray, followed by quantitative pyrosequencing validation. Large-scale data of the Cancer Genome Atlas (TCGA) were additionally reviewed. Results Unsupervised two-way hierarchical clustering using Infinium data of 21 AEG, 30 GC, and 11 NM showed four DNA MEs: extremely high-ME (E-HME), high-ME (HME), low-ME (LME), and extremely low-ME (E-LME). The promoter methylation levels were validated by pyrosequencing in 146 samples. Although almost normal mucosae were clustered into E-LME, gastric or esophagogastric junction mucosae with chronic inflammatory change due to either Helicobacter pylori infection or reflux esophagitis were clustered together into LME, which suggested that the inflammation status determined DNA MEs regardless of the causes. Three cases of Barrett’s-related adenocarcinoma were all clustered into HME. Among 94 patients whose tumors can be clustered into one of four MEs, 11 patients with E-LME cancers showed significantly shorter overall survival than the other MEs, even in multivariate Cox regression estimate. TCGA data also showed enrichment of AEG in HME and a poorer prognosis of E-LME. Conclusions E-LME cases, newly confirmed in this study, would be a unique aggressive subtype not associated with the elevation of DNA methylation levels caused by inflammation. LME could be acquired via chronic inflammation independent of the causes, and AEG frequently showed HME.

2022-10-20 | GSE207846 | GEO

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