Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The dual role of Irf1 in maintaining epithelial identity while enabling EMT [mRNA-seq]

ABSTRACT: To investigate the context-dependent function of Irf1 in maintaining epithelial identity while enabling TGFbeta-induced EMT in NMuMG/E9 cells, we downregulated Irf1 by siRNA and analyzed differentially regulated genes and pathways upon EMT induction (2 days TGFbeta) or in the absence of EMT (0 day TGFbeta). Intersection with Irf1 ChIP-sequencing after 2 days of TGFbeta treatment or in untreated cells revealed genes that are directly regulated by Irf1 and that could contribute to the dual role of Irf1 in EMT.

ORGANISM(S): Mus musculus

PROVIDER: GSE141500 | GEO | 2022/03/18

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The dual role of Irf1 in maintaining epithelial identity while enabling EMT [ChIP-seq]

Project description:To investigate the context-dependent function of Irf1 in maintaining epithelial identity while enabling TGFbeta-induced EMT in NMuMG/E9 cells, we performed chromatin immunoprecipitation with Irf1-specific antibodies in NMuMG cells treated for 2 days with TGFbeta or left untreated (0d TGFbeta). Intersection with RNA-sequencing after downregulation of Irf1 with or without treatment with TGFbeta for two days revealed genes that are directly regulated by Irf1 and that could contribute to the dual role of Irf1 in EMT.

2022-03-18 | GSE141501 | GEO

Foxf2 plays a dual role during TGFb-induced EMT by promoting apoptosis yet enabling cell junction dissolution and migration.

Project description:We have identified the transcription factor forkhead box protein F2 (Foxf2) to be upregulated in its expression during the EMT process and studied its functional contribution to EMT by siRNA-mediated knockdown in NMuMG cells treated for 4 days with TGFbeta followed by mRNA-sequencing. Our analysis revealed a dual role of Foxf2 during TGFbeta-induced EMT in promoting apoptosis while inducing cell junction breakdown and migration.

2018-10-09 | GSE112796 | GEO

Kinetic analysis of TGFbeta-induced EMT in NMuMG/E9 cells

Project description:Kinetic analysis of TGFbeta-induced EMT in NMuMG/E9 cells

| PRJNA449023 | ENA

The dual role of Irf1 in maintaining epithelial identity while enabling EMT

Project description:The dual role of Irf1 in maintaining epithelial identity while enabling EMT

| PRJNA593667 | ENA

The dual role of Irf1 in maintaining epithelial identity while enabling EMT [mRNA-seq]

Project description:The dual role of Irf1 in maintaining epithelial identity while enabling EMT [mRNA-seq]

| PRJNA593670 | ENA

The dual role of Irf1 in maintaining epithelial identity while enabling EMT [ChIP-seq]

Project description:The dual role of Irf1 in maintaining epithelial identity while enabling EMT [ChIP-seq]

| PRJNA593669 | ENA

Gene expression in epithelial, EMT (epithelial-mesenchymal transition) and MET (mesenchymal-epithelial transition) cells

Project description:NMuMG is an epithelial cell line that can be induced into EMT by TGF-β treatment or MET by TGF-β withdrawl. During EMT, several marker genes were downregulated/upregulated, which is consistent with its mesenchymal phenotype. Transcription factors that are regulated during EMT and its reverse process MET are candidate genes for the regulations of the EMT marker genes. NMuMG cells treated with vehicle, TGF-β for 11 days, or 11days of TGF-β treatment followed by TGF-β withdrawl for another 13 days. RNA from these 3 conditions of NMuMG were extracted and subject to microarray analysis

2013-07-26 | E-GEOD-48204 | biostudies-arrayexpress

Mesenchymal Epithelial Transition (MET) Timecourse of NMuMG-E9 cells treated with TGFb

Project description:Background: Epithelial-mesenchymal transition (EMT) has been implicated in metastasis, drug resistance, survival under stress and also conferring stem cell-like traits to cancer cells. However, several of the studies have been carried out using model systems that don’t appropriately recapitulate all stages of the dynamic process of EMT. Hence, there is a need to overcome this limitation by development of a model system that allows us to mimic each stage of EMT and accurately assess the plastic changes associated with it. Methods: We have derived a cancer cell line from the PyMT-MMTV model of breast cancer, named PyMT-1099 cells, and undertaken a detailed characterization of the morpho-genetic changes it undergoes during a TGFbeta-induced EMT. Further, we have also performed high throughput transcriptomics on PyMT-1099 cells undergoing EMT in a high resolution kinetic of TGFbeta treatment. Results: We show that PyMT-1099 cells undergo an EMT comparable to the classically used immortalized NMuMG cells as assessed by morphological, and marker expression changes on TGFbeta treatment. Further, PyMT-1099 cells can also migrate in vitro in response to TGFbeta treatment. These cells are also tumorigenic and lead to metastasis formation when transplanted into immunocompromised mice. Conclusion: In this study we report the development of PyMT-1099 cells as an excellent tool to model and study breast cancer-associated EMT both in vitro and in vivo and show that these cells overcome the limitations posed by other cellular systems currently being used to study EMT

2018-10-03 | GSE117474 | GEO

The dual role of Irf1 in maintaining epithelial identity while enabling EMT

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

2022-03-19 | GSE141502 | GEO

Oncogenic Ras inhibits IRF1 to promote viral oncolysis

Project description:Oncolytic viruses exploit common molecular changes in cancer cells, which are not present in normal cells, to target and kill cancer cells. Ras transformation and defects in type I interferon (IFN)-mediated antiviral responses are known to be the major mechanisms underlying viral oncolysis. Previously, we demonstrated that oncogenic RAS/Mitogen-activated protein kinase kinase (Ras/MEK) activation suppresses the transcription of many IFN-inducible genes in human cancer cells, suggesting that Ras transformation underlies type I IFN defects in cancer cells. Here, we investigated how Ras/MEK downregulates IFN-induced transcription. By conducting promoter deletion analysis of IFN-inducible genes, namely guanylate-binding protein 2 and IFN gamma inducible protein 47 (Ifi47), we identified the IFN regulatory factor 1 (IRF1) binding site as the promoter region responsible for the regulation of transcription by MEK. MEK inhibition promoted transcription of the IFN-inducible genes in wild type mouse embryonic fibroblasts (MEFs), but not in IRF1?/? MEFs, showing that IRF1 is involved in MEK-mediated downregulation of IFN-inducible genes. Furthermore, IRF1 protein expression was lower in RasV12 cells compared with vector control NIH3T3 cells, but was restored to equivalent levels by inhibition of MEK. Similarly, the restoration of IRF1 expression by MEK inhibition was observed in human cancer cells. IRF1 re-expression in human cancer cells caused cells to become resistant to infection by the oncolytic vesicular stomatitis virus strain. Together, this work demonstrates that Ras/MEK activation in cancer cells downregulates transcription of IFN-inducible genes by targeting IRF1 expression, resulting in increased susceptibility to viral oncolysis. RNA was isolated from RasV12 transformed NIH/3T3 cells (RasV12 cells) treated with 20?M U0126 or 500U/ml IFN-?, or left untreated, for 6 hours, triplicate biological samples (9 samples).

2014-11-13 | E-GEOD-49469 | 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