Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Lineage-Specific Epigenomic and Genomic Activation of Oncogene HNF4A Promotes Gastrointestinal Adenocarcinomas

ABSTRACT: Lineage-Specific Epigenomic and Genomic Activation of Oncogene HNF4A Promotes Gastrointestinal Adenocarcinomas

PROVIDER: PRJNA549160 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR9309030_1.fastq.gz	Fastqsanger.gz
	SRR9309030_2.fastq.gz	Fastqsanger.gz
	SRR9309031.fastq.gz	Fastqsanger.gz
	SRR9309032.fastq.gz	Fastqsanger.gz
	SRR9309025_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 14

Similar Datasets

Lineage-Specific Epigenomic and Genomic Activation of Oncogene HNF4A Promotes Gastrointestinal Adenocarcinomas

Project description:We profiled fresh-frozen esophageal tumor and normal samples and cell lines with chromatin immunoprecipitation sequencing (ChIP-Seq). Mathematically modeling was performed to establish (super)-enhancers landscapes and inter-connected transcriptional circuitry formed by master TFs. Coregulation and cooperation between master TFs was investigated by ChIP-Seq, RNASeq, 4C-Seq and luciferase assay. Biological functions of candidate factors were evaluated by measuring cell proliferation, colony formation, cell apoptosis and xenograft growth. Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. Here, we aim to compare of Eso26 cells knock down HNF4A with siRNA and control transcriptome profiling (RNA-seq) to microarray and quantitative reverse transcription polymerase chain reaction (qRT–PCR) methods and to evaluate protocols for optimal high-throughput data analysis. We also report the application of circular chromatin conformation capture (4C) sequencing technology for studying master transcription factor (HNF4A) in human esophageal adenocarcinoma cancer cell lines (Eso26).

2020-06-14 | GSE132813 | GEO

Oncogenic SDH mutation underlies global epigenomic instability in gastrointestinal stromal tumor

Project description:We have discovered a striking connection between mitochondrial dysfunction and epigenomic instability, manifested by global biallelic DNA cytosine 5-methylation and loss of 5-hydroxymethycytosine within succinate dehydrogenase (SDH)-null gastrointestinal stromal tumors (GIST) relative to those bearing KIT or PDGFRA tyrosine kinase driver mutations. The duality of Krebs versus kinase molecular and epigenomic profiles in GIST provides compelling evidence linking mitochondrial process to nuclear structure and function and underscores an essential role for succinate metabolism in the maintenance of epigenomic programming and tumor suppression. Bisulfite-converted DNA from 144 samples were analyzed with the Illumina GoldenGate Methylation Cancer Panel I array.

2013-05-22 | E-GEOD-34387 | biostudies-arrayexpress

HNF4A functions as an HCC oncogene or tumor suppressor depending upon the AMPK pathway activity status

Project description:Background & Aims: Hepatocyte nuclear factor 4A (HNF4A) is a master transcription factor (TF) in hepatocytes that regulates metabolism and differentiation. The mechanism of HNF4A in cancer progression remains unclear due to conflicting results observed in numerous studies. We aimed to address the roles of HNF4A in hepatocellular carcinoma (HCC). Methods: We established the HNF4A overexpression and knocking-down stable cells in HCCLM3 and Huh7, and compared the effects of HNF4A on HCC cells in different glucose supply conditions in vitro and in vivo. Pathway inhibitors treatment and phosphatase activity comparisons were performed for signaling pathway analysis. Gene levels in HCC tissues and the clinical information were collected from TCGA for survival analysis. Multiomics approaches including proteomics, TFRE and ChIP-seq were applied to identify HNF4A target genes. Rescue experiments were performed to verify the functions of the potential target genes. Results: We found HNF4A exhibited tumor-suppressive effects on proliferation and migration of HCC cells in glucose-sufficient conditions but tumor-promotive effects in glucose-insufficient conditions. This diverse functionality of HNF4A was dependent upon the AMPK pathway activity. Similarly, the prognosis predicted by HNF4A was also correlated with AMPKa expression level in HCC patients. The potential HNF4A target genes, including NEDD4 and RPS6KA2, are involved in the diverse functionality of HNF4A in response to AMPK activity status. Conclusions: The glucose supply status could be the potential decisive factor to determine functions of HNF4A on HCC cells. The switch of HNF4A between oncogene and tumor suppressor was determined by AMPK activation status, which was correlated with glucose levels.

2019-08-01 | GSE101553 | GEO

HNF4A

Project description:HNF4A

| PRJNA940175 | ENA

Oncogenic SDH mutation underlies global epigenomic instability in gastrointestinal stromal tumor

2013-05-22 | GSE34387 | GEO

Spontaneously Evolved Progenitor Niches Escape Yap Oncogene Addiction in Advanced Pancreatic Ductal Adenocarcinomas

Project description:Spontaneously Evolved Progenitor Niches Escape Yap Oncogene Addiction in Advanced Pancreatic Ductal Adenocarcinomas

| PRJNA931755 | ENA

Gene expression profiling of advanced murine K-RasG12V lung adenocarcinomas

Project description:We aimed to analyze the transcriptional profile of full-blown murine lung adenocarcinomas driven by K-RasG12V oncogene.

2015-12-14 | GSE65257 | GEO

A lineage-specific super-enhancer for MYB controls the development of gastrointestinal adenocarcinomas

Project description:A lineage-specific super-enhancer for MYB controls the development of gastrointestinal adenocarcinomas

| PRJNA980279 | ENA

Gene expression profiling of advanced murine K-RasG12V lung adenocarcinomas

Project description:We aimed to analyze the transcriptional profile of full-blown murine lung adenocarcinomas driven by K-RasG12V oncogene. We used a GEM model of lung adenocarcinoma driven by a resident K-RasG12V oncogene. On average, tumors were collected 10 months after Adeno-CRE infection.

2015-12-14 | E-GEOD-65257 | biostudies-arrayexpress

Spontaneously Evolved Progenitor Niches Escape Yap Oncogene Addiction in Advanced Pancreatic Ductal Adenocarcinomas [Cut&Tag]

Project description:Spontaneously Evolved Progenitor Niches Escape Yap Oncogene Addiction in Advanced Pancreatic Ductal Adenocarcinomas [Cut&Tag]

| PRJNA865693 | ENA