E-GEOD-48230
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA209306
PROVIDER: E-GEOD-48230 | ExpressionAtlas | 2025-01-24
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-GEOD-48230-analysis-methods.tsv | Tabular | |||
| E-GEOD-48230-analytics.tsv | Tabular | |||
| E-GEOD-48230-analytics.tsv.undecorated | Tabular | |||
| E-GEOD-48230-analytics.tsv.undecorated.unrounded | Tabular | |||
| E-GEOD-48230-analytics.tsv.unrounded | Tabular |
Items per page: 5 1 - 5 of 34 |
Similar Datasets
Project description:Transcription factors OVOL1 and OVOL2 induce the mesenchymal to epithelial transition in human cancer
| PRJNA209306 | ENA
Project description:Epithelial-to-mesenchymal transition (EMT) and cancer stem cells play relevant roles in metastasis and drug resistance in castration-resistant prostate cancer (PCa). Conditioned-media from Cancer-Associated Fibroblasts from two patients with aggressive PCa induce EMT, reversible DNA methylation and transcriptional variations in androgen independent PC3, but not in androgen dependent LN-CaP cells. Focal CpG islands hyper-methylation associated to transcriptional repression of epithelial markers occurs together with widespread hypo-methylation, including promoters of EMT and stemness regulating genes resulting in their transcriptional activation. Remarkably, DNA methylation and transcription patterns are entirely reverted upon exposure to serum-free medium (mesenchymal-to-epithelial transition). DNMT3A is required for de novo methylation and silencing of CDH1 and GRHL2, the ZEB1 direct repressor, while its knock-down prevents EMT entry. These unprecedented results highlight that CAF-released factors induce reversible DNA methylation patterns required for transcriptional variations essential for EMT and stemness in androgen independent PCa cells, suggesting that similar plasticity might occur in tumour microenvironment. This submission contains data and metadata from the methylation profiling by array of PC-3 cells treated with conditioned media from Human prostate fibroblasts (HPFs) and cancer associated fibroblasts (CAFs).
2017-03-03 | E-MTAB-4753 | biostudies-arrayexpress
Project description:Epithelial-to-mesenchymal transition (EMT) and cancer stem cells play relevant roles in metastasis and drug resistance in castration-resistant PCa. Conditioned-media from Cancer-Associated Fibroblasts from two patients with aggressive PCa induce EMT, reversible DNA methylation and transcriptional variations in androgen independent PC3, but not in androgen dependent LN-CaP cells. Focal CpG islands hyper-methylation associated to transcriptional repression of epithelial markers occurs together with widespread hypo-methylation, including promoters of EMT and stemness regulating genes resulting in their transcriptional activation. Remarkably, DNA methylation and transcription patterns are entirely reverted upon exposure to serum-free medium (mesenchymal-to-epithelial transition). DNMT3A is required for de novo methylation and silencing of CDH1 and GRHL2, the ZEB1 direct repressor, while its knock-down prevents EMT entry. These unprecedented results highlight that CAF-released factors induce reversible DNA methylation patterns required for transcriptional variations essential for EMT and stemness in androgen independent PCa cells, suggesting that similar plasticity might occur in tumour microenvironment.
2017-03-09 | E-MTAB-4752 | biostudies-arrayexpress
Project description:p63 is a transcription factor central for epithelial homeostasis and development. In our model of epithelial to mesenchymal transition (EMT) in a human prostate cell culture model, p63 was one of the most down-regulated transcription factors during EMT. We therefore investigated the role of p63 in EMT by a gain and loss of function approach. Over-expression of the predominant epithelial isoform DNp63a in mesenchymal EPT1B8 cells led to gain of several epithelial characteristics without resulting in a complete mesenchymal to epithelial transition (MET). This was corroborated by a reciprocal effect when p63 was knocked down in epithelial EP156T cells. Global gene expression analyses found that DNp63a induced gene modules involving cell adhesion genes in mesenchymal like cells. Genome-wide analysis of p63 binding sites by ChIP-seq analyses confirmed binding of p63 to regulatory areas of genes associated with cell adhesion in prostate epithelial cells.CDH1 and ZEB1 are two elemental factors in the control of EMT. Over-expression and knock-down of these factors, respectively, were not sufficient alone or in combination with DNp63a to reverse the mesenchymal phenotype in EPT1 cells. The partial reversion of epithelial to mesenchymal transition might reflect the ability of DNp63a, as a key co-ordinator of several epithelial gene expression modules, to reduce epithelial to mesenchymal plasticity (EMP). The utility of DNp63a expression and the potential of reduced EMP in order to counteract metastasis warrant further investigation. Examination of p63 binding profile in prostate cell model EP156T with EPT1 as negative control.
2013-12-20 | E-GEOD-43111 | biostudies-arrayexpress
Project description:Epithelial to Mesenchymal Transition (EMT) has been associated with cancer cell heterogeneity, plasticity and metastasis. It has been the subject of several modeling effort. This logical model of the EMT cellular network aims to assess microenvironmental signals controlling cancer-associated phenotypes amid the EMT continuum. Its outcomes relate to the qualitative degrees of cell adhesions by adherent junctions and focal adhesions, two features affected during EMT. Model attractors recover epithelial, mesenchymal and hybrid phenotypes, and simulations show that hybrid phenotypes may arise through independent molecular paths, involving stringent extrinsic signals.
Of particular interest, model predictions and their experimental validations indicated that: 1) ECM stiffening is a prerequisite for cells overactivating FAK-SRC to upregulate SNAIL1 and acquire a mesenchymal phenotype, and 2) FAK-SRC inhibition of cell-cell contacts through the Receptor Protein Tyrosine Phosphates kappa leads to the acquisition of a full mesenchymal rather than a hybrid phenotype.
2020-06-30 | MODEL2004040001 | BioModels
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.
2013-09-12 | E-GEOD-42374 | biostudies-arrayexpress
Project description:p63 is a transcription factor central for epithelial homeostasis and development. In our model of epithelial to mesenchymal transition (EMT) in a human prostate cell culture model, p63 was one of the most down-regulated transcription factors during EMT. We therefore investigated the role of p63 in EMT by a gain and loss of function approach. Over-expression of the predominant epithelial isoform DNp63a in mesenchymal EPT1B8 cells led to gain of several epithelial characteristics without resulting in a complete mesenchymal to epithelial transition (MET). This was corroborated by a reciprocal effect when p63 was knocked down in epithelial EP156T cells. Global gene expression analyses found that DNp63a induced gene modules involving cell adhesion genes in mesenchymal like cells. Genome-wide analysis of p63 binding sites by ChIP-seq analyses confirmed binding of p63 to regulatory areas of genes associated with cell adhesion in prostate epithelial cells.CDH1 and ZEB1 are two elemental factors in the control of EMT. Over-expression and knock-down of these factors, respectively, were not sufficient alone or in combination with DNp63a to reverse the mesenchymal phenotype in EPT1 cells. The partial reversion of epithelial to mesenchymal transition might reflect the ability of DNp63a, as a key co-ordinator of several epithelial gene expression modules, to reduce epithelial to mesenchymal plasticity (EMP). The utility of DNp63a expression and the potential of reduced EMP in order to counteract metastasis warrant further investigation.
2013-12-20 | GSE43111 | GEO
Project description:14 human Non-Small Cell Lung cancer (NSCLC) cell lines were treated with Transforming Growth Factor beta-1 (TGFβ-1) to induce epithelial-to-mesenchymal transition. Microarrays measured gene expression at baseline and at different times after treatment.
2019-02-13 | GSE114761 | GEO
Project description:Cellular changes during an epithelial-mesenchymal transition (EMT) largely rely on global changes in gene expression orchestrated by transcription factors. Tead transcription factors and their co-factors Yap and Taz have been shown to be implicated in EMT, nevertheless, their direct target genes during EMT have remained elusive.We used genome-wide chromatin immunoprecipitation and next generation sequencing to identify diect Tead2 target genes during EMT. Py2T cells (murine breast cancer cell line) were treated with TGFβ for 5 days and subjected to ChIP using an antibody for Tead2 followed by next generation sequencing (Illumina HiSeq 2000; n=2)
2014-03-12 | E-GEOD-55709 | biostudies-arrayexpress
Project description:Rho-GTPases are small GTP-binding proteins that contribute to the epithelial-to-mesenchymal transition by regulating several cellular processes including organization of the actin cytoskeleton, cell motility, transcription, and cell proliferation. Overexpression of RhoC-GTPases (RhoC) in breast cancer has been implicated in poor disease prognosis due to increased cancer cells invasion, migration, and motility, which warranted its consideration as a therapeutic target for inhibiting breast cancer metastasis. Using silencing RNA (siRNA) molecules to knockdown RhoC expression is a promising approach to inhibit breast cancer metastases.
2015-02-11 | ST000282 | MetabolomicsWorkbench