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MiR-1199-5p and Zeb1: a novel double-negative feedback coordinating EMT and tumour cell invasion

ABSTRACT: miR-1199-5p and Zeb1: a novel double-negative feedback coordinating EMT and tumour cell invasion

PROVIDER: PRJNA340015 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR4054990.fastq.gz	Fastqsanger.gz
	SRR4055000.fastq.gz	Fastqsanger.gz
	SRR4055010.fastq.gz	Fastqsanger.gz
	SRR4055020.fastq.gz	Fastqsanger.gz
	SRR4054991.fastq.gz	Fastqsanger.gz

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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

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

Project description:We performed miRNA-sequencing in a detailed time course of a TGFbeta-induced EMT in normal mammary gland cells and discovered 32 strongly, differentially expressed miRNAs.

2017-11-09 | GSE86025 | GEO

miR-1199-5p and Zeb1 function in a double-negative feedback loop potentially coordinating EMT and tumour metastasis.

Project description:Epithelial tumour cells can gain invasive and metastatic capabilities by undergoing an epithelial-mesenchymal transition. Transcriptional regulators and post-transcriptional effectors like microRNAs orchestrate this process of high cellular plasticity and its malignant consequences. Here, using microRNA sequencing in a time-resolved manner and functional validation, we have identified microRNAs that are critical for the regulation of an epithelial-mesenchymal transition and of mesenchymal tumour cell migration. We report that miR-1199-5p is downregulated in its expression during an epithelial-mesenchymal transition, while its forced expression prevents an epithelial-mesenchymal transition, tumour cell migration and invasion in vitro, and lung metastasis in vivo. Mechanistically, miR-1199-5p acts in a reciprocal double-negative feedback loop with the epithelial-mesenchymal transition transcription factor Zeb1. This function resembles the activities of miR-200 family members, guardians of an epithelial cell phenotype. However, miR-1199-5p and miR-200 family members share only six target genes, indicating that, besides regulating Zeb1 expression, they exert distinct functions during an epithelial-mesenchymal transition.

| S-EPMC5660124 | biostudies-literature

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-11-09 | GSE86026 | 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 and Snail1 engage miR-200f transcriptional and epigenetic regulation during EMT

2014-09-09 | GSE61217 | GEO

Mus musculus

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

| PRJNA340016 | ENA

Mus musculus

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

| PRJNA340017 | ENA

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

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

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