Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

LNK suppresses interferon signaling in melanoma

ABSTRACT: LNK suppresses interferon signaling in melanoma

PROVIDER: PRJNA524699 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR8645760.fastq.gz	Fastqsanger.gz
	SRR8645761.fastq.gz	Fastqsanger.gz
	SRR8645756.fastq.gz	Fastqsanger.gz
	SRR8645757.fastq.gz	Fastqsanger.gz
	SRR8645758.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

LNK suppresses interferon signaling in melanoma

Project description:LNK (SH2B3) is a key negative regulator of JAK-STAT signaling which has been extensively studied in malignant hematopoietic diseases. We found that LNK is significantly elevated in cutaneous melanoma; this elevation is correlated with hyperactive signaling of the RAS-RAF-MEK pathway. Elevated LNK enhances cell growth and survival in adverse conditions. Forced expression of LNK inhibits signaling by interferon-STAT1 and suppresses interferon (IFN) induced cell cycle arrest and cell apoptosis. In contrast, silencing LNK expression by either shRNA or CRISPR-Cas9 potentiates the killing effect of IFN. The IFN-LNK signaling is tightly regulated by a negative feedback mechanism; melanoma cells exposed to IFN upregulate expression of LNK to prevent overactivation of this signaling pathway. Our study reveals an unappreciated function of LNK in melanoma and highlights the critical role of the IFN-STAT1-LNK signaling axis in this potentially devastating disease. LNK may be further explored as a potential therapeutic target for melanoma immunotherapy.

2019-04-29 | GSE127333 | GEO

LNK suppresses interferon signaling in M202 melanoma cells

Project description:LNK suppresses interferon signaling in M202 melanoma cells

| PRJNA525882 | ENA

Force expression LNK suppresses interferon Gamma signaling

2019-03-31 | GSE127764 | GEO

Force expression LNK suppresses interferon Gamma signaling

Project description:Force expression LNK suppresses interferon Gamma signaling

| PRJNA525355 | ENA

LNK suppresses interferon signaling in M202 melanoma cells

Project description:LNK attenuates IFN-γ (2,000 U/ml, 24 hours) induced gene expression in M202 melanoma cells.

2019-04-30 | GSE127965 | GEO

Interferon-gamma signaling promotes melanoma progression and metastasis

Project description:To investigate the effect of Interferon-gamma signaling on gene expression in melanoma cells We performed gene expression analysis of mouse melanoma cell lines that have been treated with Interferon-gamma cytokine as compared with mock-treated controls.

2022-10-08 | GSE214873 | GEO

Interferon-gamma signaling promotes melanoma progression and metastasis

Project description:Interferon-gamma signaling promotes melanoma progression and metastasis

| PRJNA887440 | ENA

Mediator kinase inhibition suppresses hyperactive interferon signaling in Down syndrome

Project description:Mediator kinase inhibition suppresses hyperactive interferon signaling in Down syndrome

| PRJNA910594 | ENA

Mediator kinase inhibition suppresses hyperactive interferon signaling in Down syndrome II

Project description:Mediator kinase inhibition suppresses hyperactive interferon signaling in Down syndrome II

| PRJNA1049466 | ENA

Suppression of type I interferon signaling overcomes the oncogene-induced senescence and mediates melanoma development and progression

Project description:Activation of oncogenes often leads to induction of the DNA damage responses and onset of the cell senescence. Given that DNA damage can also trigger production of type I interferons (IFN) that contribute to senescence development, we sought to determine the role of IFN in the oncogene-induced senescence. Our data in mouse model demonstrate that inactivation of IFN signaling is sufficient for inducing melanomas in melanocytes harboring mutant Braf. Restoration of IFN signaling in IFN-deficient melanoma cells induces cell senescence and suppresses melanoma progression. In addition, data in human patients that received high dose IFN therapy and in mouse transplanted tumor models strongly suggest the importance of the non-cell-autonomous IFN signaling. Suppression of IFN signaling mediated by the downregulation of IFN receptor IFNAR1 invariably occurs during development of mouse melanoma. Mice harboring the IFNAR1 mutant, which is relatively resistant to downregulation, delay melanoma development, suppress the metastatic disease, and better respond to treatment with BRAF or PD1 inhibitors. These results suggest that IFN signaling is an important tumor suppressive pathway that inhibits melanoma development and progression. Accordingly, the inhibition of IFN pathway via IFNAR1 downregulation plays a key role in melanoma pathogenesis. Conversely, these data also argue for targeting IFNAR1 downregulation to prevent the metastatic disease and improve the efficacy of molecularly targeted and immune-targeted therapies. Two genotypes of mice were examined at 2 to 3 times after tamoxifen adminstration, with 2 replicates for each condition, yielding 8 samples in total.

2016-01-14 | E-GEOD-76842 | 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