Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA194616 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR799381.fastq.gz | Fastqsanger.gz | |||
| SRR799382.fastq.gz | Fastqsanger.gz | |||
| SRR799383.fastq.gz | Fastqsanger.gz | |||
| SRR799384.fastq.gz | Fastqsanger.gz | |||
| SRR799385.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 13 |
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Project description:Gene expression profiling has uncovered the transcription factor Sox4 with up-regulated activity during TGFβ-induced EMT in normal and cancerous breast epithelial cells. Sox4 is indispensable for EMT and cell survival in vitro and for primary tumor growth and metastasis in vivo. Among several EMT-relevant genes, Sox4 directly regulates the expression of Ezh2, encoding the Polycomb group histone methyltransferase that trimethylates histone 3 lysine 27 (H3K27me3) for gene repression. Ablation of Ezh2 expression prevents EMT, while forced expression of Ezh2 restores EMT in Sox4-deficient cells. Ezh2-mediated H3K27me3 marks associate with key EMT genes, representing an epigenetic EMT signature that predicts patient survival. Our results identify Sox4 as a master regulator of EMT by governing the expression of the epigenetic modifier Ezh2. Our Dataset comprises of 12 ChIP-seq samples using chromatin from NMuMG cells which was immunoprecipitated using H3K27me3-specific antibody during TGFβ-induced EMT (2ng/ml) at 6 different stages (day 0, 1, 4, 7, 10, 20).
2013-06-20 | E-GEOD-45579 | biostudies-arrayexpress
Project description:Gene expression profiling has uncovered the transcription factor Sox4 with up-regulated activity during TGFβ-induced EMT in normal and cancerous breast epithelial cells. Sox4 is indispensable for EMT and cell survival in vitro and for primary tumor growth and metastasis in vivo. Among several EMT-relevant genes, Sox4 directly regulates the expression of Ezh2, encoding the Polycomb group histone methyltransferase that trimethylates histone 3 lysine 27 (H3K27me3) for gene repression. Ablation of Ezh2 expression prevents EMT, while forced expression of Ezh2 restores EMT in Sox4-deficient cells. Ezh2-mediated H3K27me3 marks associate with key EMT genes, representing an epigenetic EMT signature that predicts patient survival. Our results identify Sox4 as a master regulator of EMT by governing the expression of the epigenetic modifier Ezh2.
2013-06-20 | GSE45579 | GEO
Project description:Epithelial to Mesenchymal Transition (EMT) renders epithelial cells to acquire migratory characteristics during development and cancer metastasis. While epigenetic and splicing changes have been implicated in EMT, the mechanisms governing their crosstalk remain poorly understood. Here, we identify C2H2 zinc finger protein, ZNF827, a novel factor, is strongly induced during important EMT mediated processes including in brain development and breast cancer metastasis and is required for the molecular and phenotypic changes underlying EMT in these processes. Mechanistically, ZNF827 mediated these responses by orchestrating a large-scale remodeling of the splicing landscape by recruiting HDAC1 for epigenetic modulation of distinct genomic loci, thereby slowing RNA Pol II progression and altering the splicing of transcripts encoding key EMT regulators in cis. These findings reveal an unprecedented complexity between epigenetic landscape and splicing and identifies ZNF827 as a master regulator coupling these processes during EMT in brain development and breast cancer metastasis.
2022-06-21 | PXD034511 | Pride
Project description:MTA1, SOX4, EZH2 and TGF-β are all potent inducers of epithelial-mesenchymal transition (EMT) in cancer; however, the signaling relationship among these molecules in EMT is poorly understood. Here, we investigated the function of MTA1 in cancer cells and demonstrated that MTA1 overexpression efficiently activates EMT. This activation resulted in a significant increase in the migratory and invasive properties of three different cancer cell lines through a common mechanism involving SOX4 activation, screened from a gene expression profiling analysis. We showed that both SOX4 and MTA1 are induced by TGF-β and both are indispensable for TGF-β-mediated EMT. Further investigation identified that MTA1 acts upstream of SOX4 in the TGF-β pathway, emphasizing a TGF-β-MTA1-SOX4 signaling axis in EMT induction. The histone methyltransferase EZH2, a component of the polycomb (PcG) repressive complex 2 (PRC2), was identified as a critical responsive gene of the TGF-β-MTA1-SOX4 signaling in three different epithelial cancer cell lines, suggesting that this signaling acts broadly in cancer cells in vitro. The MTA1-SOX4-EZH2 signaling cascade was further verified in TCGA pan-cancer patient samples and in a colon cancer cDNA microarray, and activation of genes in this signaling pathway predicted an unfavorable prognosis in colon cancer patients. Collectively, our data uncover a SOX4-dependent EMT-inducing mechanism underlying MTA1-driven cancer metastasis and suggest a widespread TGF-β-MTA1-SOX4-EZH2 signaling axis that drives EMT in various cancers. We propose that this signaling may be used as a common therapeutic target to control epithelial cancer metastasis. We used microarrays to detect MTA1-regulated genes in cancer cells.
2019-10-27 | GSE139429 | GEO
Project description:Epithelial-mesenchymal transition (EMT) is a reversible transcriptional program subverted by cancer cells to drive cancer progression. Transcription factor ZEB1 is a master regulator of EMT, driving disease recurrence in poor outcome triple negative breast cancer (TNBC). Here, we silence ZEB1 in TNBC models by CRISPR-mediated epigenetic editing, resulting in nearly complete repression of ZEB1 in vivo, accompanied by long-lasting tumor inhibition. Integrated transcriptomic and epigenetic profiling identified a ZEB1-dependent gene-signature associated with transcriptional up-regulation, promoter DNA demethylation and enhanced chromatin accessibility in core cell adhesion loci, demonstrating epigenetic reprogramming towards a more epithelial state. Epigenetic shifts induced by ZEB1-silencing are enriched in a subset of human breast tumors, illuminating a clinically-relevant hybrid-like state. Thus, the synthetic epi-silencing of ZEB1 induces stable “lock-in” epigenetic reprogramming of mesenchymal tumors associated with a distinct epigenetic landscape. We outline approaches to stably reprogram EMT for targeting poor outcome breast cancers driven by oncogenic transcription factors.
2023-04-17 | GSE210274 | GEO
Project description:Epithelial-mesenchymal transition (EMT) is a reversible transcriptional program subverted by cancer cells to drive cancer progression. Transcription factor ZEB1 is a master regulator of EMT, driving disease recurrence in poor outcome triple negative breast cancer (TNBC). Here, we silence ZEB1 in TNBC models by CRISPR-mediated epigenetic editing, resulting in nearly complete repression of ZEB1 in vivo, accompanied by long-lasting tumor inhibition. Integrated transcriptomic and epigenetic profiling identified a ZEB1-dependent gene-signature associated with transcriptional up-regulation, promoter DNA demethylation and enhanced chromatin accessibility in core cell adhesion loci, demonstrating epigenetic reprogramming towards a more epithelial state. Epigenetic shifts induced by ZEB1-silencing are enriched in a subset of human breast tumors, illuminating a clinically-relevant hybrid-like state. Thus, the synthetic epi-silencing of ZEB1 induces stable “lock-in” epigenetic reprogramming of mesenchymal tumors associated with a distinct epigenetic landscape. We outline approaches to stably reprogram EMT for targeting poor outcome breast cancers driven by oncogenic transcription factors.
2023-04-17 | GSE210276 | GEO
Project description:Epithelial-mesenchymal transition (EMT) is a reversible transcriptional program subverted by cancer cells to drive cancer progression. Transcription factor ZEB1 is a master regulator of EMT, driving disease recurrence in poor outcome triple negative breast cancer (TNBC). Here, we silence ZEB1 in TNBC models by CRISPR-mediated epigenetic editing, resulting in nearly complete repression of ZEB1 in vivo, accompanied by long-lasting tumor inhibition. Integrated transcriptomic and epigenetic profiling identified a ZEB1-dependent gene-signature associated with transcriptional up-regulation, promoter DNA demethylation and enhanced chromatin accessibility in core cell adhesion loci, demonstrating epigenetic reprogramming towards a more epithelial state. Epigenetic shifts induced by ZEB1-silencing are enriched in a subset of human breast tumors, illuminating a clinically-relevant hybrid-like state. Thus, the synthetic epi-silencing of ZEB1 induces stable “lock-in” epigenetic reprogramming of mesenchymal tumors associated with a distinct epigenetic landscape. We outline approaches to stably reprogram EMT for targeting poor outcome breast cancers driven by oncogenic transcription factors.
2023-04-17 | GSE210275 | GEO
Project description:The transcription factor SOX4 is widely expressed during development and is essential to maintain progenitor pools in a variety of organs. In breast cancer SOX4 has been shown to be associated with poor survival and increased tumor size and metastasis formation. This has mostly been attributed to the ability of SOX4 to regulate Epithelial-to-Mesenchymal-Transition (EMT). However, SOX4 regulates target gene transcription in a plastic manner that is dependent on the cellular and epigenetic context. In this study we have investigated the loss of SOX4 in mammary tumor development utilizing organoids derived from a PyMT genetic mouse model. CRISPR-mediated loss of SOX4 led to a strong impairment in growth of primary mammary tumors and subsequent metastases through an EMT-independent mechanism. Instead, SOX4 is required for inhibiting differentiation by controlling genes that are highly activated in foetal mammary stem cells (fMaSC). These SOX4-dependent genes are associated with cell cycle progression, DNA biosynthesis, RNA processing and ribosome biogenesis suggesting that SOX4 controls active cycling of tumor cells. Analysis of genes co-expressed with SOX4 in the TCGA and METABRIC studies revealed that these cell cycle-related genes correlate with SOX4 expression in human tumors. Our study identifies a novel role for SOX4 in maintaining mammary tumors in an undifferentiated proliferative state.
2021-09-30 | GSE153190 | GEO
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
Project description:This SuperSeries is composed of the following subset Series: GSE27968: DNA methylation data from AML12 cells during EMT GSE28291: Genome-scale epigenetic reprogramming during epithelial to mesenchymal transition Refer to individual Series
2011-07-03 | E-GEOD-28581 | biostudies-arrayexpress