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RNA-sequencing in MDA-231-D cells transfected with ZEB1 or ZEB2 siRNAs

ABSTRACT: We searched for roles of ZEB1and/or ZEB2 during EMT by RNA-seq in breast cancer cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE98273 | GEO | 2017/06/16

SECONDARY ACCESSION(S): PRJNA384523

REPOSITORIES: GEO

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RNA-sequencing in TGF-beta treated MDA-231-D cells transfected with ZEB1/ZEB2 siRNAs [RNA-seq]

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Project description:We searched for roles of ZEB1 during EMT through genome-wide analysis of its binding sites in breast cancer cells.

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Breast cancer MCF-7 cells and MDA-MB-231 cells: LNA-antimiR-21 transfected cells vs. LNA-control transfected cells

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Loss of ZEB2 in basal breast cancer cells

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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.

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ZEB2 protects the heart from ischemic damage

Project description:infarct size and subsequent deterioration in function. The identification of factors that enhance cardiac repair by the restoration of the vascular network is, therefore, of great significance. Here, we show that the transcription factor Zinc finger E-box-binding homeobox 2 (ZEB2) is increased in stressed cardiomyocytes and induces a cardioprotective cross-talk between cardiomyocytes and endothelial cells to enhance angiogenesis after ischemia. Single-cell sequencing indicates ZEB2 to be enriched in injured cardiomyocytes. Cardiomyocyte-specific deletion of ZEB2 results in impaired cardiac contractility and infarct healing post-myocardial infarction (post-MI), while cardiomyocyte-specific ZEB2 overexpression improves cardiomyocyte survival and cardiac function. We identified Thymosin 4 (TMSB4) and Prothymosin (PTMA) as main paracrine factors released from cardiomyocytes to stimulate angiogenesis by enhancing endothelial cell migration, and whose regulation is validated in our in vivo models. Therapeutic delivery of ZEB2 to cardiomyocytes in the infarcted heart induces the expression of TMSB4 and PTMA, which enhances angiogenesis and prevents cardiac dysfunction. These findings reveal ZEB2 as a beneficial factor during ischemic injury, which may hold promise for the identification of new therapies.

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Identification of ZEB2 binding sites in Hepatocellular Carcinoma Cell Line SNU398

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The Cdc42/Rac1 regulator CdGAP is a novel E-cadherin transcriptional co-repressor with Zeb2 in breast cancer

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2017-08-22 | GSE86301 | GEO

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