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

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

PROVIDER: PRJNA482264 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7549450.fastq.gz	Fastqsanger.gz
	SRR7549460.fastq.gz	Fastqsanger.gz
	SRR7549470.fastq.gz	Fastqsanger.gz
	SRR7549480.fastq.gz	Fastqsanger.gz
	SRR7549451.fastq.gz	Fastqsanger.gz

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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

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

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

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Mus musculus strain:NMuMg

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c-Met activation leads to the establishment of a TGFb regulatory network required for bladder cancer invasion

Project description:Aberrant c-Met activation and upregulation of its cognate ligand HGF are frequently observed in bladder cancer and have been shown to regulate downstream pathways involved in proliferation, motility, and invasion. The precise mechanism underlying HGF/c-MET mediated invasion in bladder cancer is partly addressed by this microarray dataset. HGF activates the canonical TGFb signaling pathway to enhance epithelial mesenchymal transition and bladder carcinoma invasion.

2019-08-23 | GSE104740 | GEO

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

Echovirus E9

Project description:Echovirus E9 Raw sequence reads

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

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Expression data from NMuMG-mock cells and NMuMG-MAFK cells

Project description:MAFK is one of small Maf transcripton factor famiy molecules. We found MAFK is highly expressed in several cancer cells and related to tumorigenesis. Then, we established MAFK stable cell lines using NMuMG cells (mouse mammary glad epithelium) and used microarrays to examine gene expression alteration.

2017-06-20 | GSE77956 | GEO

EPR (BC030870) ChIP-Seq analysis in NMuMG mouse mammary gland

Project description:EPR, a lncRNA present in the chromatin fraction of NMuMG cells, controls proliferation and fate determination in mammary gland cells. We wanted to define if EPR overexpression in NMuMG cells affects the landcape of two histone activation marks (H3K4me3 and H3K27ac).

2020-04-07 | GSE148182 | GEO

Identification of stable markers of the EMT:MET process

Project description:Epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) facilitate breast cancer (BC) metastasis, however stable molecular changes that result as a consequence of these processes remain poorly defined. Therefore, we sought to identify molecular markers that could distinguish tumor cells that had completed the EMT:MET cycle in the hopes of identifying and targeting unique aspects of metastatic tumor outgrowth.Therefore, normal murine mammary gland (NMumG) cells transformed by overexpression of EGFR (NME) cells were cultured in the presence of TGF-beta1 (5 ng/ml) for 4 weeks, at which point TGF-beta1 supplementation was discontinued and the cells were allowed to recover for an additional 4 weeks (Post-TGF-Rec). Total RNA was prepared from unstimulated cells (Pre-TGF) of similar passage and compared by microarray analysis. The two groups were analyzed in triplicate, three Pre-TGF samples and three Post-TGF-Rec samples.

2014-01-30 | E-GEOD-54491 | biostudies-arrayexpress

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