Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Renal cancer cell derived exosomal complement C3 promotes metastasis

ABSTRACT: Exosomal C3 derived from tumor cells promotes metastasis via recruitment of myeloid cell

ORGANISM(S): Homo Sapiens

SUBMITTER: Gao Shan

PROVIDER: PXD055611 | iProX | Fri Sep 06 00:00:00 BST 2024

REPOSITORIES: iProX

ACCESS DATA

Json Xml

Similar Datasets

exosomal ELNAT1 promotes lymphatic metastasis of bladder cancer

Project description:exosomal ELNAT1 promotes lymphatic metastasis of bladder cancer

| PRJNA657414 | ENA

Tumour derived exosomal DDAH1 promotes lung aging and metastasis

Project description:Tumour derived exosomal DDAH1 promotes lung aging and metastasis

| PRJNA1213069 | ENA

Tumor derived exosomal DDAH1 promotes lung aging and metastasis

Project description:Tumor derived exosomal DDAH1 promotes lung aging and metastasis

| PRJNA1220261 | ENA

Exosomal hsa-miR199a-3p promotes proliferation and metastasis in neuroblastoma

Project description:Exosomal hsa-miR199a-3p promotes proliferation and metastasis in neuroblastoma

| PRJNA526037 | ENA

Tumour exosomal CEMIP protein promotes cancer cell colonization in brain metastasis

Project description:Tumour exosomal CEMIP protein promotes cancer cell colonization in brain metastasis

| PRJNA562901 | ENA

Pro-survival lipid metabolism activates intracellular complement signaling to induce inflammasome-mediated tumor metastasis

Project description:Tumor metastasis remains one of the major causes of cancer-related deaths in patients with solid tumors. Mechanisms by which metabolic alterations regarding pro-survival lipid signaling activation in inducing cancer cell migration and metastasis are largely unknown. Here, we demonstrate that S1P metabolism activates endogenous complement signaling for inducing tumor metastasis via inducing inflammasome-mediated pro-inflammation. Our studies using molecular, pharmacologic and genetic tools showed that activation of sphingosine 1-phosphate (S1P) and S1P receptor 1 (S1P/S1PR1) induces tumor metastasis via enhanced intracellular complement signaling by the regulation of the C3-PPIL1 complex and subsequent inflammasome activation in cancer cells and in vivo xenograft-derived tumors.

2022-03-23 | GSE169443 | GEO

Analysis of serum exosomal miRNAs associated with lymph node metastasis in esophageal squamous cell carcinoma

Project description:Preoperative prediction of lymph node (LN) metastasis is accepted as an important independent risk factor for treatment decision-making for esophageal squamous cell carcinoma (ESCC) patients. This study aimed to develop a non-invasive biomarker to identify LN metastasis preoperatively in ESCC patients with serum exosomal RNA-seq.

2020-07-30 | GSE155360 | GEO

Cancer-derived exosomal DPP3 promotes lung metastasis by activating the RAP1 signaling pathway

Project description:Cancer-derived exosomal DPP3 promotes lung metastasis by activating the RAP1 signaling pathway

| PRJNA1194485 | ENA

Tumour exosomal CEMIP protein promotes cancer cell colonization in brain metastasis

Project description:Development of effective therapies against brain metastasis is currently hindered by limitations in our understanding of the molecular mechanisms driving it. Here we define the contributions of tumour-secreted exosomes to brain metastatic colonization and demonstrate that pre-conditioning the brain microenvironment with exosomes from brain metastatic cells enhances cancer cell outgrowth. Proteomic analysis identified cell migration-inducing and hyaluronan-binding protein (CEMIP) as elevated in exosomes from brain metastatic, but not lung or bone metastatic cells. CEMIP depletion in tumour cells impaired brain metastasis, disrupting invasion and tumour cell association with the brain vasculature, phenotypes rescued by pre-conditioning the brain microenvironment with CEMIP+ exosomes. Moreover, uptake of CEMIP+ exosomes by brain endothelial and microglial cells induced endothelial cell branching and inflammation in the perivascular niche by upregulating Ptgs2, Tnf, and Ccl/Cxcl 86 cytokines, known to promote brain vascular remodeling and metastasis. CEMIP was elevated in tumour tissues and exosomes from patients with brain metastasis and predicted brain metastasis progression and patient survival. Collectively, our findings suggest that targeting of exosomal CEMIP could constitute a future avenue for the prevention and treatment of brain metastasis.

2021-09-08 | PXD015210 | Pride

Tumour exosomal CEMIP protein promotes cancer cell colonization in brain metastasis

Project description:Development of effective therapies against brain metastasis is currently hindered by limitations in our understanding of the molecular mechanisms driving it. Here we define the contributions of tumour-secreted exosomes to brain metastatic colonization and demonstrate that pre-conditioning the brain microenvironment with exosomes from brain metastatic cells enhances cancer cell outgrowth. Proteomic analysis identified cell migration-inducing and hyaluronan-binding protein (CEMIP) as elevated in exosomes from brain metastatic, but not lung or bone metastatic cells. CEMIP depletion in tumour cells impaired brain metastasis, disrupting invasion and tumour cell association with the brain vasculature, phenotypes rescued by pre-conditioning the brain microenvironment with CEMIP+ exosomes. Moreover, uptake of CEMIP+ exosomes by brain endothelial and microglial cells induced endothelial cell branching and inflammation in the perivascular niche by upregulating Ptgs2, Tnf, and Ccl/Cxcl cytokines, known to promote brain vascular remodeling and metastasis. CEMIP was elevated in tumour tissues and exosomes from patients with brain metastasis and predicted brain metastasis progression and patient survival. Collectively, our findings suggest that targeting of exosomal CEMIP could constitute a future avenue for the prevention and treatment of brain metastasis.

2019-08-30 | GSE136628 | 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