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Expression data from Sox4 knockdown cells in the presence and absence of TGFβ in NMuMG cells

ABSTRACT: Expression profiling after Sox4 knockdown (KD) during epithelial to mesenchymal transition (EMT) in NMuMG reveals a significant number of genes that are transcriptionally deregulated.

ORGANISM(S): Mus musculus

PROVIDER: GSE44050 | GEO | 2013/06/20

SECONDARY ACCESSION(S): PRJNA188448

REPOSITORIES: GEO

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Expression data from Sox4 knockdown cells in the presence and absence of TGFÎ² in NMuMG cells

Project description:Expression profiling after Sox4 knockdown (KD) during epithelial to mesenchymal transition (EMT) in NMuMG reveals a significant number of genes that are transcriptionally deregulated. Gene expression profiling is performed in Sox4-ablated (siSox4) NMuMG cells. Cells transfected with siControl is used as a control. The cells were either treated with transforming growth factor-beta (TGFÎ²; 2ng/ml) or not.

2013-06-20 | E-GEOD-44050 | biostudies-arrayexpress

Expression data from Klf4 KD cells in the presence and absence of TGFβ in NMuMG cells

Project description:Expression profiling after Klf4 KD during EMT in NMuMG reveals a significant number of genes that are transcriptionally deregulated

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Expression data from Klf4 KD cells in the presence and absence of TGFÎ² in NMuMG cells

Project description:Expression profiling after Klf4 KD during EMT in NMuMG reveals a significant number of genes that are transcriptionally deregulated Gene expression profiling is performed in Klf4 ablated (siKlf4) NMuMG cells. Cells transfected with siControl is used as a control. The cells were either treated with TGFÎ² (2ng/ml) or not.

2013-07-24 | E-GEOD-49151 | biostudies-arrayexpress

Sox4 is a master regulator of epithelial-mesenchymal transition (EMT) by controlling Ezh2 expression and epigenetic reprogramming

Project description:Gene expression profiling has uncovered the transcription factor Sox4 with up-regulated activity during TGFÎ²-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 TGFÎ²-induced EMT (2ng/ml) at 6 different stages (day 0, 1, 4, 7, 10, 20).

2013-06-20 | E-GEOD-45579 | biostudies-arrayexpress

RNA-sequencing analysis of mouse epithelial NMuMG cells with Cas9 or UGCG knock out

Project description:We report the gene expression in mouse NMuMG cells with or without UGCG depletion using RNA sequencing. After data analysis, the 11218 transcripts were identified. Among these transcripts, the TGF-β signaling target genes and EMT marker genes were significantly upregulated in UGCG depleted NMuMG cells. Then we used these genes and mouse TGF-β or EMT gene signatures to do the gene set enrichment analysis and showed the negative correlation of UGCG and TGF-β signaling or EMT in NMuMG cells.

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Genome-wide transcripts in NMuMG cells expressing Osr2

Project description:Analysis of NMuMG cells expressing Osr2 or treated with TGF-ß. Results provide insight into a novel function of Osr2 in EMT induction.

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The prion protein contributes to epithelial-to-mesenchymal transition in the mouse NMuMG epithelial cell model

Project description:The physiological function of the prion protein (PrP) has remained elusive despite its widely recognized role in neurodegenerative diseases and sustained efforts to understand its molecular biology. On the basis of its evolutionary relationship to ZIP zinc transporters, protein-protein interactions it engages in, and the characteristics of a gastrulation arrest phenotype in a PrP-deficient model, we considered that PrP may contribute to the morphogenetic reprogramming of cells underlying epithelial-to-mesenchymal (EMT) transitions. We have conducted three global proteomics analyses to (1) identify proteins whose levels are changed during EMT in wild-type NMuMG cells; and determine proteins whose levels are affected by (2) stable knockdown or (3) transient knockdown of the prion protein relative to levels observed in wild-type NMuMG cells. We observed a highly significant correlation between proteins, which are changed during EMT or following PrP knockdown.

2015-07-10 | PXD001875 | Pride

Sox4 is a master regulator of epithelial-mesenchymal transition (EMT) by controlling Ezh2 expression and epigenetic reprogramming

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

Transcription profiling of mouse mammary epithelial cells NMuMG treatd with TGF-b1 - time series experiment

Project description:Response of mouse mammary epithelial cells NMuMG to TGF-b1 - time course experiment. Identification of novel gene targets involved in TGF-b1-driven regulation of epithelial-mesenchymal transition (EMT).

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RNA-sequencing of mouse mammary tumor organoids that were modified to generate knockout lines for SOX4

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

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