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Single cell RNA-seq and ATAC-seq of EMT induced by TGFbeta stimulation and Zeb1 overexpression

ABSTRACT: Single cell RNA-seq and ATAC-seq of EMT induced by TGFbeta stimulation and Zeb1 overexpression

PROVIDER: PRJNA471293 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7161120_1.fastq.gz	Fastqsanger.gz
	SRR7161120_2.fastq.gz	Fastqsanger.gz
	SRR7161121_1.fastq.gz	Fastqsanger.gz
	SRR7161121_2.fastq.gz	Fastqsanger.gz
	SRR7161122_1.fastq.gz	Fastqsanger.gz

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Single cell RNA-seq and ATAC-seq of EMT induced by TGFbeta stimulation and Zeb1 overexpression

Project description:We report the application of single cell RNA-sequencing using indrop on an HMLE breast cancer cell line that we induced to undergo EMT. We measured 7523 single cells after 8 and 10 days of stimulation with TGFbeta. In addition, we measured 3496 single cells in an engineered HMLE cell line with Dox inducible Zeb1, after 2 days of stimulation with Doxycycline. Finally, we performed ATAC-seq on CD44 sorted HMLE cells after 8 days of stimulation with TGFbeta.

2018-05-15 | GSE114397 | GEO

miR-1199-5p and Zeb1: a novel double-negative feedback coordinating EMT and tumour cell invasion (mRNA-seq)

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

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

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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

Kinetic analysis of TGFbeta-induced EMT in NMuMG/E9 cells

Project description:To investigate the transcriptional remodelling during EMT, we treated normal murine mammary gland epithelial cells with TGFbeta for 0, 2h, 6h, 12h, 24h, 36h, 48h, 60h, 72h, 96h, 168h and 240h. Using WGCNA and pathway enrichment analysis we identified multiple gene expression modules that were enriched in general, signaling, metabolic or stuctural pathways highly relevant for EMT.

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

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2017-11-09 | GSE86025 | GEO

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Project description:Multiple EMT-promoting/inhibiting transcription factors have been identified including Snail, Zeb1 and Ovol2. To understand differential roles of these factors, we performed gene expression profiling by RNA-seq upon Snail-/Zeb1-induced EMT or Ovol2-induced MET in human mammary epithelial MCF10A cells.

2019-07-01 | GSE70551 | GEO

Kinetic analysis of TGFbeta-induced EMT in NMuMG/E9 cells

Project description:Kinetic analysis of TGFbeta-induced EMT in NMuMG/E9 cells

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The dual role of Irf1 in maintaining epithelial identity while enabling EMT [mRNA-seq]

Project description:To investigate the context-dependent function of Irf1 in maintaining epithelial identity while enabling TGFbeta-induced EMT in NMuMG/E9 cells, we downregulated Irf1 by siRNA and analyzed differentially regulated genes and pathways upon EMT induction (2 days TGFbeta) or in the absence of EMT (0 day TGFbeta). Intersection with Irf1 ChIP-sequencing after 2 days of TGFbeta treatment or in untreated cells revealed genes that are directly regulated by Irf1 and that could contribute to the dual role of Irf1 in EMT.

2022-03-18 | GSE141500 | GEO

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