Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA340016 | ENA |
REPOSITORIES: ENA
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Project description:miR-1199-5p and Zeb1: a novel double-negative feedback coordinating EMT and tumour cell invasion
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Project description:miR-1199-5p and Zeb1: a novel double-negative feedback coordinating EMT and tumour cell invasion (mRNA-seq)
| PRJNA340017 | ENA
Project description:We investigated the effect of miR-1199-5p, miR-200b-3p and miR-429-3p on gene expression profiles during TGFbeta-induced EMT in normal murine mammary gland cells by using the mRNA-sequencing. Our analysis demonstrates that miR-1199-5p and both miR-200 family members share only 6 target genes, indicating that besides regulating Zeb1 expression they exert distinct functions during EMT.
2017-11-09 | GSE86024 | GEO
Project description:Depletion of Zeb1 in a KPC-model for pancreatic cancer affected strongly the formation of precursor lesions, tumour grading, invasion and notably metastasis during PDAC progression. In this context, EMT is important for metastasis, but there is variability and specificity (and not redundancy) in the role and function of different EMT-inducing transcription factors.
2017-03-16 | GSE87472 | GEO
Project description:EpRAS cells undergo EMT transition through hysteresis showing bistability of the system. The hysteresis transition is controlled by the negative feedback loop between miR-200s and Zeb1. Disruption of the feedback loop through the deletion of Z-box2 in the miR-200s cluster-2 promoter region changes the transition to unimodal without hysteresis. To determine the consequence of cells undergoing through hysteresis or unimodal transitions of EMT, herein we determined the transcriptomic profiles of EpRAS wild type and EpRAS-delZbox2 mutant cells, (designated as EpRAS-C2-2). To induce EMT, the cells were treated with 100pM TGFbeta for 3 days. Mock PBS treatment is used as control.
2018-11-08 | GSE106533 | GEO
Project description:Epithelial-to-mesenchymal transition (EMT) is a fundamental process in development and disease. If aberrantly activated it is a trigger for tumour progression and metastasis (Thiery et al 2009 Cell). It is now known that EMT activation is also associated with the maintenance of stem-cell properties (Mani et al. 2008 Cell). Since Zinc-finger enhancer binding transcription factor 1 (ZEB1) is a crucial EMT activator, we analyzed the changes in the gene expression profile that accompany shRNA mediated loss of ZEB1 in Panc1 pancreatic cancer cells. Panc1 is a cell line that exhibits relatively high ZEB1 levels and changes to a more benign phenotype upon ZEB1 knock down (Wellner et al. 2009 Nature Cell Biology). Panc1 cells were stably transfected with control (GFP) or ZEB1 shRNA. Upon puromycin selection, single cell clones were picked and characterized. Cells from two control versus two ZEB1 knockdown clones were harvested, total RNA was isolated and processed to hybridization.
2016-06-15 | E-MTAB-3483 | biostudies-arrayexpress
Project description:Epithelial-to-mesenchymal transition (EMT) is a fundamental process in development and disease. If aberrantly activated it is a trigger for tumour progression and metastasis (Thiery et al, 2009). It is now known that EMT activation is also associated with the maintenance of stem-cell properties (Mani et al, 2008). Since Zinc-finger enhancer binding transcription factor 1 (ZEB1) is a crucial EMT activator, we analyzed the changes in the gene expression profile that accompany siRNA mediated loss of ZEB1 in SW480 colorectal cancer cells. SW480 is a cell line that exhibits mesenchymal characteristics, but reverts to an epithelial phenotype upon ZEB1 knock down (Spaderna et al. 2006 Gastroenterology). SW480 cells were transfected with control (GFP) or ZEB1 siRNA. 72 hours after transfection, cells were harvested, total RNA was isolated and hybridized.
2016-06-15 | E-MTAB-3479 | biostudies-arrayexpress
Project description:Scaffold proteins such as CNK1 are hubs for coordinating signalling pathways. Here, we demonstrate that CNK1 is a crucial transducer of growth factor-stimulated and oncogenic signalling. Activation of CNK1 depends on its dimerization executed by the N-terminal sterile motif alpha (SAM) domain. Accordingly, a CNK1 mutant lacking the SAM domain prevents CNK1-driven cell proliferation and matrix metalloproteinase 14 promoter activation. We identified phosphorylation of Ser22 by AKT as trigger for CNK1 dimerisation. Consistently, the mutant CNK1S22D mimicking constitutive phosphorylation stimulates CNK1 signalling, whereas the phosphoylation-dead mutant CNK1S22A does not. Searching the COSMIC database revealed Ser22 as target for oncogenic activation of CNK1. The mutant CNK1S22D and the oncogenic mutant CNK1S22F form clusters in serum-starved cells comparable to clusters of CNK1 in growth factor stimulated cells. Light-activatable CNK1, optoCNK1, based on the light-induced oligomerisation of cryptochrome 2 confirms that dimerization is the trigger for CNK1 activation. CNK1 dimers induced by activating Ser22 mutants or by light enhance cell invasion and ADP ribosylation factors 1 signalling associated with tumour formation. Positive and negative feedback mechanisms regulates CNK1 dimerisation and in this way its activity. Oncogenic mutants of CNK1 support the positive feedback while escape from negative feedback regulation.
2022-02-23 | PXD003831 | Pride
Project description:Scaffold proteins such as CNK1 are hubs for coordinating signalling pathways. Here, we demonstrate that CNK1 is a crucial transducer of growth factor-stimulated and oncogenic signalling. Activation of CNK1 depends on its dimerization executed by the N-terminal sterile motif alpha (SAM) domain. Accordingly, a CNK1 mutant lacking the SAM domain prevents CNK1-driven cell proliferation and matrix metalloproteinase 14 promoter activation. We identified phosphorylation of Ser22 by AKT as trigger for CNK1 dimerisation. Consistently, the mutant CNK1S22D mimicking constitutive phosphorylation stimulates CNK1 signalling, whereas the phosphoylation-dead mutant CNK1S22A does not. Searching the COSMIC database revealed Ser22 as target for oncogenic activation of CNK1. The mutant CNK1S22D and the oncogenic mutant CNK1S22F form clusters in serum-starved cells comparable to clusters of CNK1 in growth factor stimulated cells. Light-activatable CNK1, optoCNK1, based on the light-induced oligomerisation of cryptochrome 2 confirms that dimerization is the trigger for CNK1 activation. CNK1 dimers induced by activating Ser22 mutants or by light enhance cell invasion and ADP ribosylation factors 1 signalling associated with tumour formation. Positive and negative feedback mechanisms regulates CNK1 dimerisation and in this way its activity. Oncogenic mutants of CNK1 support the positive feedback while escape from negative feedback regulation.
2022-02-23 | PXD003797 | Pride
Project description:Epithelial-to-mesenchymal transition (EMT) is a fundamental process in development and disease. If aberrantly activated it is a trigger for tumour progression and metastasis (Thiery et al 2009 Cell). It is now known that EMT activation is also associated with the maintenance of stem-cell properties (Mani et al. 2008 Cell). Since Zinc-finger enhancer binding transcription factor 1 (ZEB1) is a crucial EMT activator, we analyzed the changes in the gene expression profile that accompany shRNA mediated loss of ZEB1 in MDA MB 231 basal type breast cancer cells. MDA MB 231 is a cell line that exhibits mesenchymal characteristics, but reverts to an epithelial phenotype upon ZEB1 knock down (Spaderna et al. 2008 Cancer Research). MDA MB 231 cells were stably transfected with control (GFP) or ZEB1 shRNA. Upon puromycin selection, single cell clones were picked and characterized. Cells from two control versus two ZEB1 knockdown clones were harvested, total RNA was isolated and processed to hybridization.
2015-09-15 | E-MTAB-3482 | biostudies-arrayexpress