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Gene expression analysis in TGFbeta/TNFalpha treated A549 spheroid cultures

ABSTRACT: TGFbeta/TNFalpha treated spheroid A549 cultures are a model of the epithelial-mesenchymal transition (EMT). These experiments capture the changes in global gene expression that result from cells being induced to undergo EMT (3D control vs 3D treated), but also the differences in gene expression when A549 is grown in spheroid cultures (2D control vs 3D untreated). EMT is efficiently induced only in the spheroid culture model.

ORGANISM(S): Homo sapiens

PROVIDER: GSE42373 | GEO | 2013/09/12

SECONDARY ACCESSION(S): PRJNA181206

REPOSITORIES: GEO

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Gene expression analysis in TGFbeta/TNFalpha treated A549 spheroid cultures

Project description:TGFbeta/TNFalpha treated spheroid A549 cultures are a model of the epithelial-mesenchymal transition (EMT). These experiments capture the changes in global gene expression that result from cells being induced to undergo EMT (3D control vs 3D treated), but also the differences in gene expression when A549 is grown in spheroid cultures (2D control vs 3D untreated). EMT is efficiently induced only in the spheroid culture model. A total of 8 samples are analyzed, corresponding to 4 conditions (2D control, 2D treated, 3D control, 3D treated) and 2 biological replicates.

2013-09-12 | E-GEOD-42373 | biostudies-arrayexpress

Histone modification analysis in TGFbeta/TNFalpha treated A549 spheroid cultures

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Histone modification analysis in TGFbeta/TNFalpha treated A549 spheroid cultures

Project description:We studied the extent of chromatin remodeling in an in-vitro model of the epithelial-mesenchymal transition (EMT). EMT is induced in spheroid cultures (3D) using simultaneously two cytokines: TGFbeta and TNFalpha. The epithelial-mesenchymal transition (EMT) is a cellular de-differentiation process that has been implicated in cancer progression and metastasis. Increasing evidence suggests that EMT is regulated and established by epigenetic reprogramming, however a systems-level mechanism describing how chromatin remodeling contributes to the phenotypic switch is not known. We have generated genome-wide maps of 18 histone modifications/variants and variants in both the epithelial and mesenchymal states and quantified patterns of epigenetic changes at gene and enhancer loci. Clusters of these patterns reveal that EMT-related genes and their proximal enhancers are regulated through coordinated patterns of chromatin activation and repression at both gene and enhancer loci. At the cellular level, the remodeling of gene loci translates into a modular protein interaction network that recapitulates EMT-related signaling. Moreover, differentially activated or repressed enhancers are associated with two non-overlapping sets of transcription factors. We propose a chromatin-mediated regulatory feedback loop model where the NFkappaB and AP-1 transcription factors (TFs) bind activated enhancers, that regulate EMT-related genes, which in turn activate signaling pathways upstream of these TFs.

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Shift of EMT gradient in 3D spheroid MSCs for activation of mesenchymal niche function

Project description:This project is described about the detailed characterization of 3D spheroid mesenchymal stem cells (MSCs). Specifically, authors showed the dynamic action towards EMT in 3D MSCs and the potential of EMT-enhanced “naïve” mesenchymal phenotype.

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Homo sapiens

Project description:Gene expression analysis in TGFbeta/TNFalpha treated A549 spheroid cultures

| PRJNA181206 | ENA

Homo sapiens

Project description:Histone modification analysis in TGFbeta/TNFalpha treated A549 spheroid cultures

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Spheroid growth in ovarian cancer promotes gene expression involved in epithelial-mesenchymal transition, stem cell promotion, and multiple stress responses

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