Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion [ChIP-Seq]

ABSTRACT: 3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion [ChIP-Seq]

PROVIDER: PRJNA760457 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR15712700.fastq.gz	Fastqsanger.gz
	SRR15712701.fastq.gz	Fastqsanger.gz
	SRR15712682.fastq.gz	Fastqsanger.gz
	SRR15712683.fastq.gz	Fastqsanger.gz
	SRR15712683_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 26

Similar Datasets

3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion

Project description:3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion

| PRJNA760454 | ENA

3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion [Hi-C]

Project description:3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion [Hi-C]

| PRJNA760456 | ENA

3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion [RNA-Seq]

Project description:3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion [RNA-Seq]

| PRJNA760459 | ENA

3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion [RNA-Seq]

Project description:Epigenetic mechanisms often play an important role in driving tumor progression towards metastasis. It is less clear that deregulation of chromatin architecture, including topologically associated domains (TADS), contributes to cancer progression. CTCF is a central regulator of three dimensional chromatin structure that undergoes copy number loss in over half of all breast cancers, but the impact of this defect on epigenetic programming and chromatin architecture remains obscure. We find that the reduced pools of CTCF in hemizygous models potentiates cell invasion. Underlying this phenotype is the activation of oncogenic networks including the PI3K signaling cascade, which presents therapeutic vulnerabilities, especially to mTOR inhibitors. Deregulation of these oncogenic pathways is largely due to the loss of CTCF insulation, allowing a reorganization of long-range chromatin contacts at the subTAD level that is associated with aberrant programming of H3K27 acetylation at enhancer/promoter regions. Thus, lowered CTCF levels lead to chromatin reorganization facilitating pro-invasive transcriptional programs.

2022-01-01 | GSE183380 | GEO

3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion [ChIP-Seq]

2022-01-01 | GSE183379 | GEO

3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion [Hi-C]

2022-01-01 | GSE183378 | GEO

3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-01-01 | GSE183381 | GEO

Investigating transcriptional programs regulating invasion in basal cell carcinoma

Project description:Investigating transcriptional programs regulating invasion in basal cell carcinoma through scRNAseq analysis

2024-05-31 | GSE266665 | GEO

Investigating transcriptional programs regulating invasion in basal cell carcinoma

Project description:Investigating transcriptional programs regulating invasion in basal cell carcinoma

| PRJNA1108231 | ENA

PHGDH heterogeneity potentiates cancer cell dissemination and metastasis

Project description:Cancer metastasis requires the transient activation of cellular programs enabling dissemination and seeding in distant organs. Genetic, transcriptional and translational heterogeneity contributes to this dynamic process. Metabolic heterogeneity has also been observed, yet its role for cancer progression is less explored. Here, we discover that loss of phosphoglycerate dehydrogenase (PHGDH) potentiates metastatic dissemination. Specifically, we find that heterogeneous or low PHGDH expression in primary tumors of breast cancer patients is associated with decreased metastasis free survival time. In mice, circulating tumor cells and early metastatic lesions are enriched with PHGDH low cancer cells and silencing PHGDH in primary tumors increases metastasis formation. Mechanistically, PHGDH protein interacts with the glycolytic enzyme phosphofructokinase (PFK) and the loss of this interaction activates the hexosamine – sialic acid pathway, which provides precursors for protein glycosylation. Consequently, aberrant protein glycosylation including increased sialylation of integrin αvβ3 occurs, which potentiates cell migration and invasion. Inhibition of sialic acid metabolism counteracts the metastatic capacity of PHGDH low cancer cells. In conclusion, while the catalytic activity of PHGDH supports cancer cell proliferation, low PHGDH protein expression non-catalytically potentiates cancer dissemination and metastasis formation. Thus, the presence of PHDGH heterogeneity in primary tumors may be considered a sign of tumor aggressiveness.

2022-03-30 | GSE198380 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data