Project description:The biological process termed Epithelial-to-Mesenchymal Transition (EMT) plays a central role in cancer cell invasion, metastasis, self-renewal and resistance to therapy. Here, we characterize using chromatin immunoprecipitation and Next Generation Sequencing the genome-wide H3K9me2 distribution occurring during EMT induced by epidermal growth factor in breast cancer MDA-MB-468 cells.

2019-10-01 | GSE121662 | GEO

Role of iron in the regulation of the epithelial-to-mesenchymal transition (RNA-seq)

Project description:The biological process termed Epithelial-to-Mesenchymal Transition (EMT) plays a central role in cancer cell invasion, metastasis, self-renewal and resistance to therapy1,2. Here, we characterize using RNA sequencing the mRNA levels changes occurring during EMT induced by epidermal growth factor in breast cancer MDA-MB-468 cells. 1. Nieto, M. A., Huang, R. Y., Jackson, R. A. & Thiery, J. P. EMT: 2016. Cell 166, 21–45 (2016). 2. Puisieux, A. & Brabletz, T. & Caramel, J. Oncogenic roles of EMT-inducing transcription factors. Nat. Cell Biol. 16, 488–494 (2014).

2019-10-01 | GSE121663 | GEO

Role of TERRA lncRNA during epithelial-to-mesenchymal transition

Project description:We analyzed the contribution of TERRA lncRNA in an invitro model of epithelial-to-mesenchymal transition induced by TGFβ.

2019-03-28 | GSE97110 | GEO

The role of LSD1 in Epithelial to Mesenchymal Transition

Project description:The role of LSD1 in Epithelial to Mesenchymal Transition

| PRJNA413779 | ENA

Role of TGFi1 in epithelial to mesenchymal transition (EMT)

Project description:Role of TGFi1 in epithelial to mesenchymal transition (EMT)

| PRJNA778227 | ENA

TP63 regulation of epithelial to mesenchymal transition in an experimental prostate cell model

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

Epithelial to mesenchymal transition shed microvesicle proteome

Project description:Epithelial-mesenchymal transition (EMT) is a highly conserved morphogenic process defined by the loss of epithelial characteristics and the acquisition of a mesenchymal phenotype. EMT is associated with increased aggressiveness, invasiveness, and metastatic potential in carcinoma cells. To assess the contribution of extracellular vesicles following EMT, we conducted a proteomic analysis of shed microvesicles released from Madin-Darby canine kidney (MDCK) cells, and MDCK cells transformed with oncogenic H-Ras (21D1 cells).

2021-03-18 | PXD022290 | Pride

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