Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Acquisition of CCDC88A/GIV through Tumor-Stroma Tunnels Promotes Aggressive Phenotypes of Estrogen Receptor-Positive Breast Cancer [dataset3]

ABSTRACT: Acquisition of CCDC88A/GIV through Tumor-Stroma Tunnels Promotes Aggressive Phenotypes of Estrogen Receptor-Positive Breast Cancer [dataset3]

PROVIDER: PRJNA930632 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR23314786.fastq.gz	Fastqsanger.gz
	SRR23314787.fastq.gz	Fastqsanger.gz
	SRR23314788.fastq.gz	Fastqsanger.gz
	SRR23314789.fastq.gz	Fastqsanger.gz
	SRR23314790.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 9

Similar Datasets

Acquisition of CCDC88A/GIV through Tumor-Stroma Tunnels Promotes Aggressive Phenotypes of Estrogen Receptor-Positive Breast Cancer.

Project description:Acquisition of CCDC88A/GIV through Tumor-Stroma Tunnels Promotes Aggressive Phenotypes of Estrogen Receptor-Positive Breast Cancer.

| PRJNA930630 | ENA

Acquisition of CCDC88A/GIV through Tumor-Stroma Tunnels Promotes Aggressive Phenotypes of Estrogen Receptor-Positive Breast Cancer [dataset1]

Project description:Acquisition of CCDC88A/GIV through Tumor-Stroma Tunnels Promotes Aggressive Phenotypes of Estrogen Receptor-Positive Breast Cancer [dataset1]

| PRJNA930631 | ENA

Acquisition of CCDC88A/GIV through Tumor-Stroma Tunnels Promotes Aggressive Phenotypes of Estrogen Receptor-Positive Breast Cancer [dataset2]

Project description:Acquisition of CCDC88A/GIV through Tumor-Stroma Tunnels Promotes Aggressive Phenotypes of Estrogen Receptor-Positive Breast Cancer [dataset2]

| PRJNA930633 | ENA

Acquisition of CCDC88A/GIV through Tumor-Stroma Tunnels Promotes Aggressive Phenotypes of Estrogen Receptor-Positive Breast Cancer [dataset3]

Project description:Estrogen receptor-positive (ER+) breast cancer commonly disseminates to bone marrow, where interactions with mesenchymal stromal cells (MSCs) shape disease trajectory. We modeled these interactions using tumor-MSC co-cultures and using an integrated transcriptome-proteome-network-analyses workflow identified a comprehensive catalog of contact-induced changes. Induced genes/proteins—some borrowed and others tumor-intrinsic response—were not recapitulated merely by conditioned media. Protein-protein interaction networks reveal the rich connectome between the ‘borrowed’ and ‘intrinsic’ components. Bioinformatic analyses helped prioritize one of the ‘borrowed’ components, CCDC88A/GIV, a bona-fide multi-modular metastasis-related protein. MSCs upregulated GIV in ER+ breast cancer cells through connexin (Cx)43-facilitated intercellular long-distance transport. Stable expression of GIV recapitulated ~20% of both the ‘borrowed’ and the ‘intrinsic’ gene induction patters observed during contact cocultures, conferred resistance to clinical anti-estrogen drugs, and enhanced tumor dissemination. These data provide a multiomic insight into the role of MSC→tumor cell intercellular transport and validate as proof-of-concept how transport of one such candidate, GIV, from the haves (MSCs) to have-nots (ER+ breast cancer) orchestrates aggressive disease states.

2024-06-21 | GSE224321 | GEO

Acquisition of CCDC88A/GIV through Tumor-Stroma Tunnels Promotes Aggressive Phenotypes of Estrogen Receptor-Positive Breast Cancer [dataset2]

2024-06-21 | GSE224320 | GEO

Acquisition of CCDC88A/GIV through Tumor-Stroma Tunnels Promotes Aggressive Phenotypes of Estrogen Receptor-Positive Breast Cancer [dataset1]

2024-06-21 | GSE224319 | GEO

A multi-omic analysis implicates the acquisition of CCDC88A/GIV through tumor-stroma tunnels in escape from tumor cell dormancy

Project description:Estrogen receptor-positive (ER+) breast cancer commonly disseminates to bone marrow, where interactions with mesenchymal stromal cells (MSCs) shape disease trajectory. Using a co-culture model, we performed an integrated transcriptomic and proteomic analysis of processes induced in ER+ breast cancer cells by close contact with MSCs, but not merely by conditioned media. Computational approaches identified a 52-protein/mRNA ‘signature’ which stratified patients at high risk for relapse, and implicated long-distance intercellular transport via tunneling nanotubes (TNTs) as a means for their ‘acquisition’ by the tumor cell from MSCs. Bioinformatic analyses helped prioritize one gene/protein, CCDC88A/GIV, a multi-functional adapter protein known to drive metastasis. MSCs upregulated GIV in ER+ breast cancer cells through connexin 43-mediated intercellular transport. Stable expression of GIV conferred resistance to clinical anti-estrogen drugs, enhanced tumor dissemination, and recapitulated the 52-gene signature. These data establish a new multi-omic resource for the regulation of breast cancer by MSCs via intercellular transport and validate as proof-of-concept how one transported protein, GIV, orchestrates aggressive disease states.

2024-07-02 | PXD039860 | Pride

Acquisition of CCDC88A/GIV through Tumor-Stroma Tunnels Promotes Aggressive Phenotypes of Estrogen Receptor-Positive Breast Cancer.

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

2024-06-21 | GSE224322 | GEO

TLR4 signaling and macrophage inflammatory responses are dampened by GIV/Girdin

Project description:Sensing of pathogens by Toll-like receptor 4 (TLR4) induces an inflammatory response; controlled responses confer immunity but uncontrolled responses cause harm. Here we define how a multi-modular scaffold, GIV (a.k.a Girdin) titrates such inflammatory response in macrophages. Upon challenge with microbe-derived lipopolysaccharides (LPS, a ligand for TLR4), macrophages with GIV mount a more tolerant (hypo-reactive) transcriptional response and suppress pro-inflammatory cytokines and signaling pathways (i.e., NFkB and CREB) downstream of TLR4 compared to their GIV-depleted counterparts.

2020-07-08 | GSE153924 | GEO

GIV/Girdin Regulates Spatiotemporal Signaling during Sperm Capacitation and is Required for Male Fertility

Project description:For a sperm to successfully fertilize an egg, it must first undergo capacitation in the female reproductive tract, and later undergo acrosomal reaction (AR) upon encountering an egg. How premature AR is avoided despite rapid surges in signaling cascades during capacitation remains unknown. Using a combination of KO mice and cell-penetrating peptides, here we show that GIV (CCDC88A), a guanine nucleotide-exchange factor (GEM) for trimeric GTPases, is highly expressed in spermatocytes and is required for male fertility. GIV is rapidly phosphoregulated on key tyrosine and serine residues in human and murine sperms. These phosphomodifications enable GIV-GEM to orchestrate two distinct compartmentalized signaling programs in the sperm tail and head; in the tail, GIV enhances PI3K→Akt signals, sperm motility and survival, whereas in the head it inhibits cAMP surge and premature AR. Furthermore, GIV transcripts are downregulated in the testes and semen of infertile men. These findings exemplify the spatiotemporally segregated signaling programs that support sperm capacitation and the etiology of infertility in men.

2021-08-16 | GSE171704 | 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