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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE190095 | GEO | 2022/03/14

REPOSITORIES: GEO

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Transcriptome analysis in treated MCF7-V breast carcinoma cell line stably expressing 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. In MCF7-V cells, we used RNA-seq to study the impact of ZEB1 on the ERα transcriptome in breast cancer cells induced with DMSO, 17-beta estradiol (E2), and forskolin + 3-isobutyl-1-methylxanthine (IBMX) (FI).

2022-03-14 | GSE173484 | 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.

2022-03-14 | GSE173491 | GEO

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).

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Systems level analysis of epithelial to mesenchymal transition reveals more alteration in phosphoproteome than proteome and identifies DNAJB4 and CD81 as EMT regulators

Project description:We quantified protein expression changes between epithelial and mesechymal stages in immortalized human mammary epithelial cells (HMLE). Epithelial–mesenchymal transition is induced by expressing an EMT-TF, Twist.

2019-06-24 | PXD012001 | Pride

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

Candidate ERalpha targets for DNA methylation-mediated gene silencing

Project description:DNA methylation of specific CpG sites associates with estrogen receptor α (ERα)-positive status in human breast cancer. Therefore, ERα may regulate gene expression in part via DNA methylation. This hypothesis was tested in a panel of antihormone-resistant T47D and MCF-7 cells with varying levels of ERα expression/activity that were derived by long-term fulvestrant treatment and by estrogen deprivation. Using Agilent’s Whole Human Genome 4x44K v2 gene expression microarrays, the intersection of ERα inversely-related genes and genes induced by the DNA methyltransferase-inhibitor decitabine were identified and revealed 39 candidate ERα DNA methylation targets. Enrichment analysis indicated over-representation of ERα-binding sites, basal-up/luminal-down markers, cancer stem cell genes, epithelial-mesenchymal transition (EMT) genes, inflammatory genes and tumor suppressors. Kaplan-Meier survival curve and Cox proportional hazard regression analyses indicated these candidate targets predicted poor distant metastasis-free survival among 2,116 breast cancer patients. The basal and EMT genes LCN2 and IFI27 showed the greatest inverse relationship with ERα expression/activity and contain ERα-binding sites, therefore they were selected for validation. LCN2 and IFI27 CpG methylation levels, quantitated by pyrosequencing, were inversely related to ERα expression/activity in wild-type and antihormone-resistant ERα-negative T47D cells, in ERα-negative T47D cells infected with lentiviral ERα, and in a panel of 11 breast cancer cell lines. Implications: ERα directs DNA methylation-mediated silencing of specific genes, such as basal markers, and thereby may in part program breast cancers as the prognostically more favorable luminal subtype. Thus, genes that can be methylated in an ERα-dependent manner may serve as predictive biomarkers in breast cancer.

2017-02-05 | GSE85536 | GEO

RAS-induced transformation of mammary epithelial cells relies on ZEB1-dependent cellular reprogramming through a paracrine process

Project description:The distinct frequency of activation of the RAS/MAPK signaling pathway in human cancers suggests a context-dependent cellular state of vulnerability to RAS transformation. While uncommon in breast cancers, oncogenic activation of this pathway is frequent in claudin-low (CL) tumors, a subtype of breast malignancies enriched in features of epithelial-mesenchymal transition (EMT), suggesting an interplay between RAS activation and EMT. Using inducible models of human mammary epithelial cells, we show that RAS-mediated transformation relies upon cellular reprogramming governed by the EMT-inducing transcription factor ZEB1. The path to ZEB1 induction involves a paracrine process: cells entering a senescent state following RAS induction release proinflammatory cytokines, notably IL-6 and IL1 which promote ZEB1 expression and activity in neighboring cells, thereby fostering their malignant transformation. Collectively, our findings unveil a previously unprecedented role for senescence in bridging RAS activation and EMT over the course of malignant transformation of human mammary epithelial cells.

2024-02-16 | GSE201536 | GEO

Cancer-associated E239K mutation of LSD1 promotes the migration and invasion of luminal breast cancer cells by reducing the expression of ERα

Project description:Background: Epithelial to mesenchymal transition (EMT) plays an essential role in the metastasis of breast cancer by regulating the migration and invasion of cancer cells. Lysine specific demethylase 1 (LSD1) is an important histone demethylase that mediates EMT. However, the functional effects of the mutation on LSD1 in breast cancer remain unclear. Results: An E239K mutation of LSD1 was identified from TCGA Breast Invasive Carcinoma cohort. To investigate the functional effects of the E239K mutation of LSD1, a stable LSD1 knockdown MCF7 cell line was generated. Rescue with the wild-type LSD1, but not the E239K mutated LSD1, suppressed the increased invasion of the LSD1 knockdown cells, demonstrating that the E239K mutation abolished the suppressive effects of LSD1 on the invasion of breast cancer cells. Further analysis showed that the E239K mutation of LSD1 led to decreased expression of estrogen receptor α (ERα), which subsequently increased the expression of Slug, a master transcription factor that promoted EMT. Most importantly, the E239K mutation of LSD1 disrupted the interaction between LSD1 and GATA3, which reduced the enrichment of LSD1 at the promoter region of ERα gene. The reduced enrichment of LSD1 at the promoter region of ERα gene caused enhanced histone H3K9 methylation, which in turn suppressed the transcription of ERα gene. Conclusions: The E239K mutation of LSD1 promotes the migration and invasion of breast cancer cells by disrupting the interaction between LSD1 and GATA3, which reduces the expression of ERα by enhancing the histone H3K9 methylation.

2021-03-12 | GSE168706 | GEO

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

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

| PRJNA785831 | ENA