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The EMT-regulator ZEB1 shapes bone marrow immunological niches in AML suppressing T-cell activity and fostering Th17 expansion

ABSTRACT: We performed gene expression profiling to evaluate potential differences between Zeb1 expressing and Zeb1 silenced cells

ORGANISM(S): Mus musculus

PROVIDER: GSE192473 | GEO | 2022/12/21

REPOSITORIES: GEO

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The EMT-regulator ZEB1 shapes bone marrow immunological niches in AML suppressing T-cell activity and fostering Th17 expansion

Project description:The EMT-regulator ZEB1 shapes bone marrow immunological niches in AML suppressing T-cell activity and fostering Th17 expansion

| PRJNA791633 | ENA

ZEB1 is regulated by K811 acetylation to promote stability, NuRD complex interactions, EMT, and NSCLC metastasis

Project description:To understand the role of Zeb1 acetylation in regulating its function a Zeb1 acetyl-mimetic and acetyl-deficient mutant expressing NSCLC cell line was generated. We then performed gene expression profiling analysis using data obtained from RNA-seq of GFP-vector, Zeb1 wild-type, Zeb1 deficient, and Zeb1 mimetic.

2023-08-09 | GSE225400 | GEO

Zeb1 and Snail1 engage miR-200f transcriptional and epigenetic regulation during EMT

Project description:Cell plasticity is emerging as a key regulator of tumor progression and metastasis. During carcinoma dissemination epithelial cells undergo epithelial to mesenchymal transition (EMT) processes characterized by the acquisition of migratory/invasive properties, while the reverse, mesenchymal to epithelial transition (MET) process, is also essential for metastasis outgrowth. Different transcription factors, called EMT-TFs, including Snail, bHLH and Zeb families are drivers of the EMT branch of epithelial plasticity, and can be post-transcriptionally downregulated by several miRNAs, as the miR-200 family. The specific or redundant role of different EMT-TFs and their functional interrelations are not fully understood. To study the interplay between different EMT-TFs, comprehensive gain and loss-of-function studies of Snail1, Snail2 and/or Zeb1 factors were performed in the prototypical MDCK cell model system. We here describe that Snail1 and Zeb1 are mutually required for EMT induction while continuous Snail1 and Snail2 expression, but not Zeb1, is needed for maintenance of the mesenchymal phenotype in MDCK cells. In this model system, EMT is coordinated by Snail1 and Zeb1 through transcriptional and epigenetic downregulation of the miR-200 family. Interestingly, Snail1 is involved in epigenetic CpG DNA methylation of the miR-200 loci, essential to maintain the mesenchymal phenotype. The present results thus define a novel functional interplay between Snail and Zeb EMT-TFs in miR200f regulation providing a molecular link to their previous involvement in the generation of EMT process in vivo. Expression analysis of MDCK over-expression EMT-TF Analysis of 7 overexpression MDCK cells each of them using biological rpelicates (MDCK-E47, Snail2, Snail1, Twist1, Tiwst2, Zeb1, Zeb2)

2014-09-09 | E-GEOD-61217 | biostudies-arrayexpress

Zeb1-mediated control of PUFA-phospholipids in EMT/plasticity-associated cancer cell ferroptosis

Project description:Therapy resistance and metastasis, the most fatal steps in cancer, are often triggered by a (partial) activation of the epithelial-mesenchymal-transition (EMT)-program. A mesenchymal phenotype predisposes to ferroptosis, a cell death pathway exerted by an iron and oxygen-radical mediated peroxidation of phospholipids containing polyunsaturated fatty acids (PUFAs). We here describe that various forms of EMT-activation, including TGFB-stimulation, increase ferroptosis-susceptibility in cancer cells, which depends on the EMT-transcription factor Zeb1. Among other effects, we demonstrate that Zeb1 increases the ratio of phospholipids containing pro-ferroptotic PUFAs over cyto-protective monounsaturated fatty acids (MUFAs) and modulates the expression of underlying crucial lipogenic enzymes (and ACSL4). Pharmacological inhibition of selected lipogenic enzymes (SCD and FADS2) allows the manipulation of ferroptosis-sensitivity in a Zeb1-dependent manner. Our data are of potential translational relevance and suggest a combination of ferroptosis-activators and SCD-inhibitors for the treatment of aggressive cancers expressing Zeb1, which might also be a useful predictive marker for such a combination therapy

2024-07-05 | GSE264671 | GEO

Zeb1 and Snail1 engage miR-200f transcriptional and epigenetic regulation during EMT

2014-09-09 | GSE61217 | GEO

Transcriptome analysis studying the role of ZEB1 in Th1 and Th17 differentiation [RNA-seq]

Project description:We performed bulk-RNAseq to study the role of ZEB1 in human and mouse Th1 and Th17 cells differentiation.

2021-07-12 | GSE179832 | GEO

microRNA-seq analysis studying the role of ZEB1 in Th0 and Th17 differentiation [miRNA-seq]

Project description:We performed microRNA-seq to study the role of ZEB1 in human Th17 cells differentiation.

2021-07-12 | GSE179834 | GEO

The EMT-activator Zeb1 is crucial for cellular plasticity and drives metastasis in pancreatic cancer

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

ChIP-seq NS5 Zeb1

Project description:ChIP-seq NS5 Zeb1

| PRJEB9360 | ENA

ZEB1-regulated inflammatory phenotype in breast cancer cells

Project description:This SuperSeries is composed of the SubSeries listed below. Zinc finger E-box binding protein 1 (ZEB1) and ZEB2 induce epithelial-mesenchymal transition (EMT) and cancer progression. However, little is known about global picture of transcriptional regulation by ZEB1 and ZEB2. Here we identified an inflammatory phenotype regulated by ZEB1 using chromatin immunoprecipitation-sequencing (ChIP-seq) and RNA-sequencing (RNA-seq) in basal type breast cancer cells, followed by gene set enrichment analysis (GSEA) of ZEB1-bound genes.

2017-06-16 | GSE89206 | GEO

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