Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

NECTIN1 controls an IGF1-dependent adhesion switch in melanoma spreading

ABSTRACT: NECTIN1 controls an IGF1-dependent adhesion switch in melanoma spreading

PROVIDER: PRJNA628861 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11624228_1.fastq.gz	Fastqsanger.gz
	SRR11624228_2.fastq.gz	Fastqsanger.gz
	SRR11624229_1.fastq.gz	Fastqsanger.gz
	SRR11624229_2.fastq.gz	Fastqsanger.gz
	SRR11624230_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

NECTIN1 controls an IGF1-dependent adhesion switch in melanoma spreading

Project description:Defects in cell-cell contacts have been proposed to participate in early steps of tumor metastasis1 but little is known about the signals from the cancer cell niche that influence this process. Here, we show that the lack of adherens junctions caused by genetic loss of the adhesion molecule NECTIN1 in melanoma promotes tumor dissemination specifically under growth factor deprivation. We found that NECTIN1 was deleted in 53% of human melanomas and that its loss was enriched in metastases. NECTIN1 inactivation in zebrafish melanomas stimulated cancer cell spreading in vivo, while in human cell lines, it increased cell migration specifically in response to serum starvation. We further identified IGF1 as the serum component responsible for this effect. Serum withdrawal or IGF1 inhibition induced formation of strong adherens junctions between NECTIN1-wild-type melanoma cells. In contrast, NECTIN1-deficient cells were unable to establish adherens junctions and instead activated integrin-mediated motility through a FAK/SRC axis. During melanoma dissemination, NECTIN1 loss thus causes a cellular phenotypic switch from cell-cell adhesion to cell-matrix adhesion triggered by IGF1 signaling. Our study uncovers a mechanism by which cancer cells integrate information from the tumor microenvironment and cell-cell contacts to regulate their migratory behavior during spreading.

2022-05-26 | GSE149481 | GEO

Frequent loss of adhesion gene NECTIN1 triggers melanoma dissemination upon local IGF1 depletion [RNA-Seq]

Project description:Defects in cell-cell contacts participate in early steps of tumor metastasis, but the mechanism regulating the staying-at-home or leaving decision has not been molecularly defined. We found the adherens junction gene NECTIN1 deleted in 55% of human melanomas. Inactivation of NECTIN1 stimulated cancer cell spreading in zebrafish melanomas in vivo, and increased cell migration in human cell lines specifically in response to decreased IGF1 signaling. IGF1 inhibition induced robust formation of adherens junctions between NECTIN1-wildtype melanoma cells, while NECTIN1-deficient cells were unable to establish these junctions and instead activated integrin/FAK-mediated motility. In 20 human melanoma biopsies, adherens junctions were seen exclusively in areas with low IGF1 levels, but not in NECTIN1-deficient tumors. Our study uncovers a mechanism by which the status of cell-cell contacts modulates the cellular response to microenvironmental signals, effecting a decision switch between leaving and staying in the cancer cell niche.

2022-05-26 | GSE174149 | GEO

Frequent loss of adhesion gene NECTIN1 triggers melanoma dissemination upon local IGF1 depletion

Project description:Frequent loss of adhesion gene NECTIN1 triggers melanoma dissemination upon local IGF1 depletion

| PRJNA728590 | ENA

Generating IGF1 signatures in human melanoma cell lines by activation of IGF1 or ihibition of IGF1R

Project description:To generate IGF1 signatures in human melanoma cell lines. Recombinant human IGF1 (rhIGF1) was added to WM35, known to be responsive to rhIGF1, whereas constitutive IGF1 signaling in Mel-624 was abrogated by siRNA directed against the IGF1 receptor (siIGF1R). Experiments were performed in triplicate in normoxia (O2 concentration, 21%) and hypoxia (1% O2), because hypoxia has been suspected to play an adverse role in melanoma. After generating GEP data, we created signatures of genes significantly (p ≤0.0001, q ≤0.05) and consistently upregulated in rhIGF1-treated WM35 cells, or similarly downregulated in siIGF1R-treated Mel-624 cells, as compared to control cells at the same O2 concentration.

2018-01-01 | GSE59343 | GEO

Frequent loss of adhesion gene NECTIN1 triggers melanoma dissemination upon local IGF1 depletion [RNA-Seq]

Project description:Frequent loss of adhesion gene NECTIN1 triggers melanoma dissemination upon local IGF1 depletion [RNA-Seq]

| PRJNA728593 | ENA

Serum IGF1 is a new prognostic marker for resistance to targeted therapies and a predictive marker for anti-IGF1R therapy in melanoma

Project description:In a prospective clinical study, we show that increased serum IGF1 levels in a patient may be a predictive marker of melanoma escape to therapies targeting MAPK pathway (BRAFi/MEKi). In addition, our in vitro and in vivo studies suggest that the response of targeted therapies-resistant melanoma cells to IGF1R inhibitor appears to correlate with the level of IGF1 secretion. Overall, our results suggest that monitoring serum IGF1 levels would individually identify melanoma patients who escape BRAFi/MEKi treatment and may benefit from a combination of targeted therapies and IGF1 signaling inhibition to overcome resistance.

2023-10-30 | GSE239284 | GEO

Expression data from E18.5 Igf1 -/- (homozygous mutant) and Igf1+/+ (normal wild type control) mouse lungs

Project description:Insight into the role of Insulin-like Growth Factor (IGF) in development of lungs has come from the study of genetically modified mice. IGF1 is a key factor during lung development. IGF1 deficiency in the neonatal mouse causes respiratory failure collapsed alveoli and altered alveolar septa. To further characterize IGF1 function during lung development we analyzed Igf1-/- mouse prenatal lungs in a C57Bl/6 genetic background. Mutant lungs showed disproportional hypoplasia, disorganized extracellular matrix and dilated alveolar capillaries. IGF1 target genes during lung maturation were identified by analyzing RNA differential expression in Igf1-/- lungs using microarrays. Lungs from E18.5 were isolated from both Igf1+/+ wild type and Igf1-/- null mice and pooled to obtain RNA. Heterozygous male and female with a genetic background C57BL/6J were mated to obtain embryos at embrionic (E) stage 18.5 days post coitum (E18.5). 3 biological replicates per genotype.

2014-03-31 | E-GEOD-17157 | biostudies-arrayexpress

MITF reprograms the extracellular matrix and focal adhesion in melanoma

Project description:MITF reprograms the extracellular matrix and focal adhesion in melanoma

| PRJNA686997 | ENA

AKT1E17K activates focal adhesion kinase and promotes melanoma brain metastasis

Project description:AKT1E17K activates focal adhesion kinase and promotes melanoma brain metastasis

| PRJNA507777 | ENA

Clinical relevance of SKP2 alterations in metastatic melanoma

Project description:Melanoma cell lines were genotyped to evaluate copy number differences between nodular melanoma (NM) and superficial spreading melanoma (SSM). Cell lines were also evaluated for copy number alterations in the SKP2/p27 axis. Affymetrix SNP arrays were performed according to manufacturer's instructions using DNA extracted from 18 melanoma cell lines and 4 melanocyte controls. Affymetrix SNP6.0 Array data for melanoma cell lines Copy number analysis of Affymetrix SNP 6.0 arrays was performed on 18 melanoma cell lines including 2 primary superficial spreading melanoma, 2 primary nodular melanoma, 2 metastatic nodular melanoma, and 12 metastatic cell lines. Four melanocyte control lines were also evaluated including 2 immortalized melanocyte cell lines (Hermes 1 and 2B) and 2 normal melanocyte lines cultured from neonatal foreskin (HEM-N and HEM-LP) that were used to construct the baseline for copy number analysis.

2010-10-21 | E-GEOD-22305 | 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