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ZEB1 binding sites in TGF-beta-stimulated MCF7 breast cancer cell line

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

ORGANISM(S): Homo sapiens

PROVIDER: GSE98270 | GEO | 2017/06/16

SECONDARY ACCESSION(S): PRJNA384522

REPOSITORIES: GEO

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ZEB1 binding sites in TGF-beta-stimulated MDA-231-D and Hs578T basal type breast cancer cell lines [ChIP-seq]

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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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ChIP-seq of ZEB1 in MCF7-V breast carcinoma cell line transduced with a doxycyline-inducible construct to express ZEB1

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Transcriptome analysis in treated MCF7-V breast carcinoma cell line stably expressing a doxycyline-inducible construct to express ZEB1.

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ChIP-seq of estrogen receptor α in wild type MCF7-V and in MCF7-V breast carcinoma cell line transduced with a doxycyline-inducible construct to express ZEB1.

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. We did ERα ChIP-seq in wild type MCF7-V cells for comparative studies. We also did ERα ChIP-seq in cells stably expressing a doxycycline-inducible construct to express ZEB1. This was to determine the impact of ZEB1 on the ERα cistrome in MCF7-V breast cancer cells induced with DMSO, 17-beta estradiol (E2), and forskolin + 3-isobutyl-1-methylxanthine (IBMX) (FI).

2022-03-14 | GSE173479 | GEO

Single cell analysis of MCF7-V breast carcinoma cell line stably expressing a doxycyline-inducible construct to express ZEB1 in presence of dxycycline.

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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Inhibition of ZEB1 expression induces redifferentiation of adult human β cells expanded in vitro

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-mesenchymal transition (EMT) involves profound changes in cell morphology, driven by transcriptional and epigenetic reprogramming. However, it emerges that translation and the ribosome composition play also key role in establishing physio-pathological phenotypes. Using genome-wide analyses, we report significant rearrangement of the translational landscape and machinery during EMT. Specifically, a mesenchymal cell line overexpressing the EMT transcription factor ZEB1 shows alterations in translational reprogramming and fidelity. Considering the change in translational activity of ZEB1-overexpressing mesenchymal cells, including in fidelity activity, we sought for changes in ribosome composition. We thus performed a riboproteome approach, i.e., mass spectrometry (MS)-based quantitative proteomic analysis of purified cytoplasmic ribosomes to highlight any change in relative amount of individual ribosomal proteins between wild-type and ZEB1-overexpressing human mammary epithelial cells.

2024-11-02 | PXD047409 | Pride

Defining the role of ZEB1 in the pathogenesis of lung cancer

Project description:Using an in vitro model for malignant transformation of human bronchial epithelial cells (HBECs) we have found epithelial-to-mesenchymal transition (EMT) and expression of the EMT-transcription factor ZEB1 are early and critical events. Specifically, we found preexisting oncogenic mutations in TP53 and KRAS were required for HBECs to engage EMT machinery in response to microenvironmental (serum/TGFβ) or specific oncogenetic (MYC) EMT-inducing factors, which induce EMT through distinct TGFβ-dependent and vitamin D receptor (VDR)-dependent pathways, respectively, with both requiring ZEB1. Functional studies demonstrated ZEB1 causally promotes the malignant progression of HBECs and tumorigenicity of NSCLC and small cell lung cancer (SCLC) lines. Mechanistically ZEB1 directly represses ESRP1 leading to increased mesenchymal splicing of CD44, which drives a switch to CD44hi status and defines a highly transformed subpopulation. This was supported by finding ZEB1 is expressed in early-stage primary non-small cell lung cancers (NSCLC), as early as stage IB tumors, and its expression correlates with TNM stage. We conclude that: ZEB1-induced EMT and associated ESRP1 and CD44 molecular changes are important biomarkers for lung cancer pathogenesis; TGFβ and VDR are EMT chemoprevention targets; and as such, ZEB1 represents an important therapeutic target in NSCLC and SCLC.

2016-08-31 | GSE77925 | 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

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