Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification of endothelial derived factors that promote metastasis II

ABSTRACT: Identification of endothelial derived factors that promote metastasis II

PROVIDER: PRJNA606604 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11085357.fastq.gz	Fastqsanger.gz
	SRR11085358.fastq.gz	Fastqsanger.gz
	SRR11085359.fastq.gz	Fastqsanger.gz
	SRR11085360.fastq.gz	Fastqsanger.gz
	SRR11085361.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Identification of endothelial derived factors that promote metastasis I

Project description:Identification of endothelial derived factors that promote metastasis I

| PRJNA606750 | ENA

Identification of endothelial derived factors that promote metastasis III

Project description:Identification of endothelial derived factors that promote metastasis III

| PRJNA606757 | ENA

Identification of endothelial derived factors that promote metastasis II

Project description:To identify endothelial-derived factors that may instructively drive cancer metastasis, we generated a new mouse model that allows endothelial-specific ribosomal tagging. We crossed the RiboTag (Rpl22fl/flHA) mice with the endothelial inducible Cre line Cdh5(PAC)-CreERT2 mice. Endothelial derived ribosome-associated mRNA-sequencing was performed from highly metastatic B16F10 and poorly metastatic B16F0 tumours.

2020-06-29 | GSE145291 | GEO

Identification of endothelial derived factors that promote metastasis III

2020-06-29 | GSE145317 | GEO

Identification of endothelial derived factors that promote metastasis I

2020-06-29 | GSE145293 | GEO

Glucocorticoids Promote Breast Cancer Metastasis

Project description:Glucocorticoids Promote Breast Cancer Metastasis

| PRJNA513860 | ENA

Blood flow diverts extracellular vesicles from endothelial degradative compartments to promote angiogenesis

Project description:Extracellular vesicles released by tumors (tEVs) disseminate via circulatory networks and promote microenvironmental changes in distant organs favoring metastatic seeding. Despite their abundance in the bloodstream, how hemodynamics affect the function of circulating tEVs remains unsolved. We experimentally tuned flow profiles in vitro (microfluidics) and in vivo (zebrafish) and demonstrated that efficient uptake of tEVs occurs in endothelial cells subjected to capillary-like hemodynamics. Such flow profiles partially reroute internalized tEVs towards non-acidic and non-degradative Rab14-positive endosomes, at the expense of lysosomes, suggesting that endothelial mechanosensing diverts tEVs from degradation. Subsequently, tEVs promote the expression of pro-angiogenic transcription factors in flow-stimulated endothelial cells and favor vessel sprouting in zebrafish. Altogether, we demonstrate that capillary-like flow profiles potentiate the pro-tumoral function of circulating tEVs by promoting their uptake and rerouting their trafficking. We propose that tEVs contribute to pre-metastatic niche formation by exploiting endothelial mechanosensing in specific vascular regions with permissive hemodynamics. This set of experiments represents RNAseq of HUVEC cells subjected to 400 µm/s flow versus no flow (static conditon).

2023-07-11 | E-MTAB-13156 | biostudies-arrayexpress

Identification of endothelial derived factors in highly metastatic tumours

Project description:Identification of endothelial derived factors in highly metastatic tumours

| PRJNA606753 | ENA

Immune suppressive effects of radiotherapy promote metastasis

Project description:Immune suppressive effects of radiotherapy promote metastasis

| PRJNA960856 | ENA

Endothelial inhibition of the glycolytic activator PFKFB3 induces tumor vessel normalization, impairs metastasis and improves chemotherapy

Project description:Abnormal tumor vessels promote metastasis and impair chemotherapy. Hence, tumor vessel normalization (TVN) by targeting endothelial cells (ECs) is emerging as anti-cancer treatment. Here, we show that tumor ECs (TECs) have a hyper-glycolytic metabolism, shunting glycolytic intermediates to nucleotide synthesis. EC haplo-deficiency or blockade of the glycolytic activator PFKFB3 did not affect tumor growth, but reduced cancer cell intra- and extravasation and metastasis by normalizing tumor vessels, which improved vessel maturation and perfusion. Mechanistically, PFKFB3 inhibition tightened the vascular barrier by reducing VE-cadherin endocytosis in ECs and rendering glycolytic pericytes more quiescent; it also lowered the expression of cancer cell adhesion molecules in ECs. Additionally, PFKFB3-blockade treatment improved chemotherapy. Considering TEC metabolism for anti-cancer treatment might thus merit further attention.

2016-11-17 | E-MTAB-4842 | biostudies-arrayexpress

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