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Expression data from MCF7 cells treated with Neuregulin (NRG) at different times

ABSTRACT: To gain insights into the mechanism responsible for the protumorigenic actions of NRG we performed gene expression analyses of MCF7 cells treated with soluble NRG for 3, 6, 12 and 24 hours.

ORGANISM(S): Homo sapiens

PROVIDER: GSE69540 | GEO | 2015/06/04

SECONDARY ACCESSION(S): PRJNA285811

REPOSITORIES: GEO

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Expression data from MCF7 cells treated with Neuregulin (NRG) at different times

Project description:To gain insights into the mechanism responsible for the protumorigenic actions of NRG we performed gene expression analyses of MCF7 cells treated with soluble NRG for 3, 6, 12 and 24 hours. MCF7 cells were treated with NRG for 0, 3, 6,12, 24 hours, 3 for each condition, prepared from three different experiments

2015-06-04 | E-GEOD-69540 | biostudies-arrayexpress

Characterization of the effect of deleting the Nrg-1(neuregulin-1) gene, using the endothelial driver line Tie2-Cre in E (embryonic day) 9.5 hearts

Project description:To investigate the role of Nrg-1 in heart ventricular chamber development we deleted Nrg-1 in endothelial lineages, harvested hearts at E9.5, and determined gene expression profiles, using RNA-seq.

2023-12-01 | GSE216470 | GEO

Characterization of the effect of overexpressing the Nrg-1 (neuregulin-1) gene, using the cardiac driver line Nkx2.5-Cre, in E (embryonic day) 15.5 heart venticles

Project description:To investigate the role of Nrg-1 in heart ventricular chamber development, we overexpressed Nrg-1 in cardiac lineages, harvested ventricles at E15.5, and determined gene expression profiles, using RNA-seq.

2023-12-01 | GSE216467 | GEO

Characterization of the effect of deleting the Nrg-1(neuregulin-1) gene, using the tamoxifen-inducible endothelial driver line Cdh5-CreERT in E (embryonic day) 15.5 hearts

Project description:To investigate the role of Nrg-1 in heart ventricular chamber development, we induced a conditional Nrg-1 deletion in endothelial cells at E15.5, with tamoxifen, and determined gene expression profiles, using RNA-seq.

2023-12-01 | GSE216469 | GEO

Role of Nrg-1 in the development of heart ventricular chamber in mice.

Project description:To investigate the role of Nrg-1 in heart ventricular chamber development, we have used RNA-Seq to characterize the effect of Nrg-1 inactivation or over-expression in mouse embryos at E9.5 and E15.5. This SuperSeries is composed of the SubSeries listed below.

2023-12-01 | GSE216471 | GEO

Escherichia coli O83:H1 str. NRG 857C

Project description:Escherichia coli O83:H1 str. NRG 857C genome sequencing project

| PRJNA41221 | ENA

Infarcted rats teated with rhNRG-1(recombinant human NRG-1)

Project description:The ErbB famliy of erceptor tyrosine kinases and their ligands, neuregulins(NRGs), are crtical involved not only in cardiac development but also in the maintenace of structural and functional integrity of the adult heart. rhNRG-1(recombinant human NRG-1) Improves cardiac function and sruvival in models of ischemic, dilated, and viral cardiomyopathy with the ErbB-activation. But the mechanism is still unknown Keywords: Genechips

2007-10-18 | GSE9263 | GEO

NRG-1 induces mature ventricular cardiac differentiation from iPS cells contributing to cardiac tissue repair

Project description:Combined treatment with NRG-1 and DMSO led to efficient differentiation of iPS into mature ventricular-like cardiac cells, which were capable of preserving cardiac function and tissue viability when transplanted into a mouse model of myocardial infarction.

2017-03-24 | GSE56511 | GEO

2D-PAGE coupled with nLC-MS/MS-based identification of differentialy expressed proteins and tumorigenic pathways in MCF7 breast cancer cell line transfected for JTB protein silencing

Project description:Identification of new cancer-associated genes/proteins, characterization of their expression vari-ation, the interactomics-based assessment of differentially expressed genes/proteins (DEGs/DEPs), and understanding the tumorigenic pathways and biological processes involved in BC genesis and progression are necessary and possible by rapid and recent advances in bioin-formatics and molecular profiling strategies. Taking into account the opinion of other authors, as well as based on our own team’s in vitro studies, we sustain that JTB protein might be consid-ered as a tumor biomarker for BC and should be studied as a target for BC therapy. In this study we have identified the differentially expressed proteins (DEPs), carcinogenic pathways and bio-logical processes associated with JTB silencing, using 2D-PAGE coupled with nano-liquid chro-matography tandem mass spectrometry (nLC-MS/MS) proteomics applied to MCF7 breast cancer cell line, for complementing and completing our previous results based on SDS-PAGE, as well as in-solution proteomics of MCF7 cells transfected for JTB downregulation. The functions of significant DEPs have been analysed using GSEA and KEGG analysis. Almost all DEPs exert protumorigenic effects in JTBlow condition, sustaining the tumor suppressive function of JTB. Thus, the identified DEPs are involved in several signaling and metabolic pathways that exert protumorigenic roles: EMT, ERK/MAPK, PI3K/AKT, Wnt/β-catenin, mTOR, C-MYC, NF-κB, IFN-γ and IFN-α response, UPR, and glycolysis/gluconeogenesis. These pathways sustain cancer cell growth, adhesion, survival, proliferation, invasion, metastasis, resistance to apoptosis, cytoskeleton reorganization, maintenance of stemness, metabolic reprogramming, survival into a hostile environment, and a poor clinical outocome. In conclusion, JTB silencing might increase the neoplastic phenotype and behavior of MCF7 BC cell line.

2024-01-26 | PXD046265 | Pride

MCF-7 Cell Derived Soluble Factors Define Growth of Vascular and Lymphatic Endothelial Cells: Modulatory Role of miR193a

Project description:Angiogenesis and Lymphangiogenesis plays a key role in promoting tumor growth and breast cancer progression as well as metastasis. Active angiogenic process within the tumor tissue is known to promote cancer/tumor growth via nutrient supply, moreover, soluble molecules secreted by lymphatic endothelial cells (ECs) promotes tumor growth. Hence is feasible that paracrine factors generated by breast cancer cells play a role in regulating tumor neovascularization by lymphatic and vascular ECs. Here using cultured VECs and LECs assessed the paracrine impact of MCF-7 breast cancer derived soluble factors on LEC and VEC growth (cell number), gene expression (micro array) and angiogenic proteins (protein array). Moreover, we explored the modulatory actions of miR193 on LEC and VEC growth driven by MCF-7 derived conditioned medium (MCF7-CM). We demonstrate that MCF7-CM differentially modulates VEC and LEC growth, i.e. induces VEC growth and inhibits LEC growth. Moreover, the growth actions of MCF7-CM were accompanied with differential modulation VEC and LEC growth regulatory genes, that were further altered by miR193 a pretreatment of MCF7 cells. Our findings provide in-depth analysis of MCF7-CM altered genes relevant for angiogenesis and lymphogenesis. The fact that vascular capillaries support growth and lymphatic capillaries play a role counteracting cancer growth (kill cancer cells), together with our observation in VECs and LECs, suggests that MCF-7 breast cancer cells differentially modulate vascular and lymphatic growth to facilitate their survival and growth. Since miR193a abrogates the effects of MCF7-CM, it may be an effective therapeutic tool against breast cancer.

2022-07-13 | GSE189084 | GEO

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