ZEB1 binding sites in TGF-beta-stimulated MCF7 breast cancer cell line
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE98270 | GEO | 2017/06/16
SECONDARY ACCESSION(S): PRJNA384522
REPOSITORIES: GEO
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Project description:The epithelial to mesenchymal transition (EMT) is implicated in the metastatic spread of breast cancer cells. EMT transcription factors (TF) regulate different stages of EMT states. In breast cancers, estrogen receptor α (ERα) maintains the epithelial characteristics of breast tumors and is indispensable for efficient endocrine therapy. In this study we investigate whether and how ZEB1, an EMT-TF affects ERα signaling at early stages of EMT and metastasis. In MCF7-V cells, we performed scRNA-seq to evaluate if ZEB1 modulates cellular heterogeneity at early EMT states in breast cancer cells.
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Project description:In-vitro expansion of functional adult human β-cells is an attractive approach for generating insulin-producing cells for transplantation. However, human islet cell expansion in culture results in loss of β-cell phenotype and epithelial-mesenchymal transition (EMT). This process activates expression of ZEB1 and ZEB2, two members of the zinc-finger homeobox family of E-cadherin repressors, which play key roles in EMT. Downregulation of ZEB1 using shRNA in expanded β-cell-derived (BCD) cells induced mesenchymal-epithelial transition (MET), β-cell gene expression, and proliferation attenuation. In addition, inhibition of ZEB1 expression potentiated redifferentiation induced by a combination of soluble factors, as judged by an improved response to glucose stimulation and a 3-fold increase in the fraction of C-peptide-positive cells to 60% of BCD cells. Furthermore, ZEB1 shRNA led to increased insulin secretion in cells transplanted in vivo. Our findings suggest that the effects of ZEB1 inhibition are mediated by attenuation of the miR-200c target genes SOX6 and SOX2. These findings, which were reproducible in cells derived from multiple human donors, emphasize the key role of ZEB1 in EMT in cultured BCD cells and support the value of ZEB1 inhibition for BCD cell redifferentiation and generation of functional human β-like cells for cell therapy of diabetes.
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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.
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