E-GEOD-54505
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA252884PRJNA236738
PROVIDER: E-GEOD-54505 | ExpressionAtlas | 2019-05-14
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:TWIST1-induced microRNA-424 drives an intermediate epithelial-to-mesenchymal transition that opposes metastasis
| PRJNA252884 | ENA
Project description:TWIST1-induced microRNA-424 drives an intermediate epithelial-to-mesenchymal transition that opposes metastasis
| PRJNA236738 | ENA
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:Extracellular pH (pHe) is lower in many tumors than in the corresponding normal tissue. Acidic tumor microenvironment has been shown to facilitate epithelial mesenchymal transition (EMT) and tumor metastasis, while the mechanisms underlying tumor acidic microenvironment-induced tumor cell metastasis remain undefined. Here, we aimed to investigate the tumor metastasis and the EMT by acidic microenvironment and to explore their mechanisms and clinical significance in lung cancer. Results showed that acidic pHe remarkably enhanced invasion ability of lung cells accompanying with increased mesenchymal and decreased epithelial markers. Moreover, acidic pHe triggered the inhibition of microRNA-7 (miR-7) expression and activation of TGF-β2/SMAD signaling. Mechanistic studies showed that TGF-β2 is a direct potential target gene of miR-7, and acidity-induced metastasis could be abolished by treatment with a TGFβRI inhibitor, anti-TGF-β2 antibody and miR-7 mimic, respectively. The clinical samples further revealed that miR-7 was decreased in lung tissues and antagonistically correlated with TGF-β2 expression, associating with overall survival and metastasis. In conclusion, our study indicated that acidic pHe showed enhanced invasive potential, and enhanced potential to develop experimental metastases by a novel mechanism involving tumor acidic microenvironment-induced regulation of miR-7/TGF-β2/SMAD axis. Our findings suggest that the possibility that pHe of the primary tumor may be an important prognostic parameter for lung cancer patients merit clinical investigation. Moreover, miR-7 may serve as prognostic molecular marker and a novel therapeutic target for lung cancer.
2022-04-01 | PXD016524 | Pride
Project description:This SuperSeries is composed of the following subset Series: GSE39356: MiR-374a Promotes Epithelial-Mesenchymal Transition (EMT) and Metastasis of Breast Cancer (mRNA dataset) GSE39358: MiR-374a Promotes Epithelial-Mesenchymal Transition (EMT) and Metastasis of Breast Cancer (miRNA dataset) Refer to individual Series
2012-07-13 | E-GEOD-39359 | 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) is a dynamic process that relies on cellular plasticity; an EMT/MET axis is critical for metastatic colonization of carcinomas. Unlike epithelial programming, regulation of mesenchymal programming is not well understood in EMT. Here we describe the first microRNA that enhances exclusively mesenchymal programming. We demonstrate that microRNA-424 is up-regulated early during a TWIST1/SNAI1-induced EMT, and that it causes cells to express mesenchymal genes without affecting epithelial genes, resulting in a mixed/intermediate EMT. Further, microRNA-424 increases motility, decreases adhesion and induces a growth arrest, changes associated with a complete EMT. Patient microRNA-424 levels positively associate with TWIST1/2 and EMT-like gene signatures and is increased in primary tumors versus matched normal breast. However, microRNA-424 is down-regulated in metastases versus matched primary tumors. Correspondingly, microRNA-424 decreases tumor initiation and is post-transcriptionally down-regulated in macrometastases in mice. RNA-seq identified microRNA-424 regulates numerous genes associated with EMT and breast cancer stemness including the novel miR-424 target, TGFBR3, which regulates mesenchymal phenotypes without influencing miR-424 effects on tumor-initiating phenotypes; instead, we show that ERK signaling is critical for such tumor-initiating effects of miR-424. These findings suggest microRNA-424 plays distinct roles downstream of EMT-inducing factors, facilitating earlier stages, but repressing later stages, of metastasis. Examination of mRNA levels in MCF12A human breast cell lines that stably over-expressed miR-424 or an empty vector (EV) control. Each group has three replicates.
2015-02-26 | E-GEOD-54505 | biostudies-arrayexpress
Project description:DCBLD2 Mediates Epithelial-Mesenchymal Transition-Induced Metastasis by Cisplatin in Lung Adenocarcinoma
| PRJNA707567 | ENA
Project description:Notch2 in promotion of bladder cancer growth and metastasis through epithelial to mesenchymal transition (EMT), cell cycle progression and maintenance of stemness. Notch2 induced gene expression in human urinary bladder cancer was measured at three independent experiments.
2014-08-21 | E-GEOD-60564 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE32694: Transcriptome and microRNA array analyses reveal a stimulatory effect of the phytochemical shikonin on epithelial–mesenchymal transition (EMT) in mouse skin [gene expression profile] GSE32695: Transcriptome and microRNA array analyses reveal a stimulatory effect of the phytochemical shikonin on epithelial–mesenchymal transition (EMT) in mouse skin [microRNA expression profile] Refer to individual Series
2011-12-31 | E-GEOD-32696 | biostudies-arrayexpress