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RNA-sequencing of EpH4 and EpRas cells treated with Etv4 and Etv5 siRNAs and/or TGF-beta.

ABSTRACT: We performed RNA-seq analysis in mouse mammary gland epithelial EpH4 cell line and its Ras-transformed derivative (EpRas) to analyze the mechanisms of transcriptional regulation during TGF-beta-induced EMT.

ORGANISM(S): Mus musculus

PROVIDER: GSE69363 | GEO | 2017/04/10

SECONDARY ACCESSION(S): PRJNA285319

REPOSITORIES: GEO

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FAIRE-seq analysis of Ras transformed mouse mammary gland epithelial cells transfected with Etv4 and Etv5 siRNAs and stimulated with TGF-beta.

Project description:We performed global mapping of accessible chromatin in mouse mammary gland epithelial EpH4 cell line and its Ras-transformed derivative (EpRas) using formaldehyde-assisted isolation of regulatory element (FAIRE)-sequencing (seq) to analyze the mechanisms of transcriptional regulation during TGF-beta-induced EMT.

2017-04-10 | GSE94977 | GEO

Dynamics of chromatin accessibility during TGF-beta-induced EMT of Ras-transformed mammary gland epithelial cells [FAIRE-Seq]

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Dynamics of chromatin accessibility during TGF-beta-induced EMT of Ras-transformed mammary gland epithelial cells

Project description:This SuperSeries is composed of the SubSeries listed below. Epithelial-mesenchymal transition (EMT) is induced by transforming growth factor (TGF)-beta stimulation and facilitates tumor progression. We here performed global mapping of accessible chromatin in the mouse mammary gland epithelial EpH4 cell line and its Ras-transformed derivative (EpRas) using formaldehyde-assisted isolation of regulatory element (FAIRE)-sequencing (seq). We also searched for differentially expressed transcription factors by RNA-seq and found that Etv4, an ETS family oncogenic transcription factor, was strongly expressed in EpRas cells. Moreover, chromatin immunoprecipitation (ChIP)-seq showed that Etv4 bound to more than one-third of the accessible chromatin regions in EpRas cells treated with TGF-beta. We found by gene ontology analysis that genes encoding extracellular proteins are the most strongly down-regulated genes by Etv4 and Etv5 siRNAs. These findings suggest a mechanism of transcriptional regulation during TGF-beta-induced EMT that involves alterations of accessible chromatin.

2017-04-10 | GSE69387 | GEO

Etv4 and Etv5 binding sites in EpRas mouse mammary gland epithelial cell line [ChIP-seq]

Project description:We searched for roles of Etv4 and Etv5 during EMT through genome-wide analysis of their binding sites in Ras-transformed mammary gland epithelial cells.

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Gene expression analysis of EpH4 cell monolayers following TGF-β3 treatment

Project description:EpH4 cell monolayers were treated with 1 ng/ml TGF-β3 or vehicle for 24 hours. The experiment was performed three independent times, with 3 wells per condition in each experiment. Keywords: Expression profiling by array

2015-10-01 | GSE62126 | GEO

Gene expression of EpH4 cells stably transfected with PR

Project description:Whole mouse genome analysis to discover differentially expressed genes in EpH4 cells overexpressing PR Total RNA was extracted from stably transfected EpH4-PR mouse epithelial cell line

2011-07-13 | E-GEOD-30637 | biostudies-arrayexpress

Gene expression of EpH4 cells stably transfected with PR

Project description:Whole mouse genome analysis to discover differentially expressed genes in EpH4 cells overexpressing PR

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Expression profiling of EpH4 mouse mammary epithelial cells overexpressing the AP-1 transcription factor component Fra1

Project description:RNA of control mouse mammary epithelial cells (EpH4 control) and corresponding fra1 overexpressing cells (EpH4fra1 cl1 and EpH4fra1 cl2) was hybridized onto an 53MM chip and differentially expressed targets were further analysed. For each sample hybridization was performed in technical triplicate

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ETV4 and ETV5 drive synovial sarcoma through cell cycle and DUX4 embryonic pathway control.

Project description:Synovial sarcoma is an aggressive malignancy with no effective treatments for patients with metastasis. The synovial sarcoma fusion SS18-SSX, which recruits the SWI/SNF-BAF chromatin remodeling and polycomb repressive complexes, results in epigenetic activation of FGF receptor (FGFR) signaling. In genetic FGFR-knockout models, culture, and xenograft synovial sarcoma models treated with the FGFR inhibitor BGJ398, we show that FGFR1, FGFR2, and FGFR3 were crucial for tumor growth. Transcriptome analyses of BGJ398-treated cells and histological and expression analyses of mouse and human synovial sarcoma tumors revealed prevalent expression of two ETS factors and FGFR targets, ETV4 and ETV5. We further demonstrate that ETV4 and ETV5 acted as drivers of synovial sarcoma growth, most likely through control of the cell cycle. Upon ETV4 and ETV5 knockdown, we observed a striking upregulation of DUX4 and its transcriptional targets that activate the zygotic genome and drive the atrophy program in facioscapulohumeral dystrophy patients. In addition to demonstrating the importance of inhibiting all three FGFRs, the current findings reveal potential nodes of attack for the cancer with the discovery of ETV4 and ETV5 as appropriate biomarkers and molecular targets, and activation of the embryonic DUX4 pathway as a promising approach to block synovial sarcoma tumors.

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Etv4 and Etv5 are required downstream of GDNF and Ret for kidney branching morphogenesis.

Project description:Glial cell line-derived neurotrophic factor signaling through the Ret receptor tyrosine kinase is crucial for ureteric bud branching morphogenesis during kidney development, yet few of the downstream genes are known. Here we show that the ETS transcription factors Etv4 and Etv5 are positively regulated by Ret signaling in the ureteric bud tips. Mice lacking both Etv4 alleles and one Etv5 allele show either renal agenesis or severe hypodysplasia, whereas kidney development fails completely in double homozygotes. We identified several genes whose expression in the ureteric bud depends on Etv4 and Etv5, including Cxcr4, Myb, Met and Mmp14. Thus, Etv4 and Etv5 are key components of a gene network downstream of Ret that promotes and controls renal branching morphogenesis.

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