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

ORGANISM(S): Mus musculus

SUBMITTER: Neha Tiwari

PROVIDER: E-GEOD-44050 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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

Tiwari Neha N Tiwari Vijay K VK Waldmeier Lorenz L Balwierz Piotr J PJ Arnold Phil P Pachkov Mikhail M Meyer-Schaller Nathalie N Schübeler Dirk D van Nimwegen Erik E Christofori Gerhard G

Cancer cell 20130601 6

Gene expression profiling has uncovered the transcription factor Sox4 with upregulated activity during TGF-β-induced epithelial-mesenchymal transition (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 ...[more]

PMID: 23764001

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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

TGF-Î² Tumor Suppression Through A Lethal EMT

Project description:TGF-Î² is a major tumor suppressor in gastrointestinal (GI) and squamous carcinomas, which exhibit frequent genetic inactivation of Smad4, a key TGF-Î² signaling component. Apoptosis is implicated as an important mediator of the tumor suppressive function of TGF-Î², although this process remains poorly understood. To address this long-standing question, we dissected the tumor suppressive action of TGF-Î² in naÃ¯ve pancreatic ductal adenocarcinoma (PDA) cells. Here we show that TGF-Î²/Smad4 signaling triggers an EMT in Kras-mutant pancreatic progenitor cells but turns this process into a trigger of apoptosis by converting the progenitor cell transcription factor Sox4 from an enforcer of epithelial progenitor identity into an activator of apoptosis. This occurs as a result of the EMT-linked repression of the endodermal master regulator Klf5, which cooperates with Sox4 to promote epithelial progenitor identity, and loss of which unmasks a latent apoptotic transcriptional program driven by Sox4. By losing Smad4, Kras-mutant PDA cells avoid this fate and instead use Sox4 as a TGF-Î²-dependent enforcer of the epithelial progenitor cell state. In this study, 16 RNA-Seq samples and 6 ChIP-Seq samples are included.

2016-02-24 | E-GEOD-72069 | biostudies-arrayexpress

SOX4 AND SMARCA4 COOPERATIVELY REGULATE PI3K SIGNALING THROUGH TRANSCRIPTIONAL ACTIVATION OF TGFBR2 IN TRIPLE NEGATIVE BREAST CANCER

Project description:Dysregulation of PI3K/Akt signaling is a dominant feature in basal-like or triple-negative breast cancers (TNBC). However, the mechanisms regulating this pathway are largely unknown in this subset of aggressive tumors. Here we demonstrate that the transcription factor SOX4 is a key regulator of PI3K signaling in TNBC. Genomic and proteomic analyses coupled with mechanistic studies identified TGFBR2 as a direct transcriptional target of SOX4 and demonstrated that TGFBR2 is required to mediate SOX4-dependent PI3K signaling. We further report that SOX4 and the SWI/SNF ATPase SMARCA4, which are uniformly overexpressed in basal-like tumors, form a previously unreported complex that is required to maintain an open chromatin conformation at the TGFBR2 regulatory regions in order to mediate TGFBR2 expression and PI3K signaling. Collectively, our findings delineate the mechanism by which SOX4 and SMARCA4 cooperatively regulate PI3K/Akt signaling and suggest that this complex may play an essential role in TNBC genesis and/or progression. Kinase enrichment proteomic analysis was performed using HCC1143 breast cancer cells treated with a control siRNA pool or a pool targeting SOX4 in biological triplicate to evaluate the effects on the functional kinome.

2021-03-03 | PXD022596 | Pride

ChIP-Seq of Klf4 in NMuMG normal murine mammary gland epithelial cells.

Project description:Chromatin immunoprecipitation of Klf4 in NMuMG cells identifies gene promoter sequences that are directly bound by Klf4. Chromatin immunoprecipitation using a Klf4-specific antibody in NMuMG cells followed by next generation sequencing (ChIP-Seq).

2013-08-01 | E-GEOD-49445 | biostudies-arrayexpress

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

2013-06-20 | GSE44050 | GEO

siRNA profiling of human LNCaP cells transfected with SOX4 cDNA, SOX4 siRNA or GFP cDNA

Project description:SOX4 is a critical developmental transcription factor in vertebrates and is required for precise differentiation and proliferation in multiple tissues. In addition, SOX4 is overexpressed in many human malignancies, but the precise role of SOX4 in cancer progression is not well understood. Here we have either eliminated SOX4 using siRNA or overexpressed a SOX4 cDNA and compared the gene expression patterns against control GFP transfections to identify SOX4 target genes. Data described in manuscript P. Liu et al., Cancer Res 46, 4011 (April 15, 2006) Experiment Overall Design: LNCaP prostate cancer cells were transfected with either a SOX4 cDNA, a pool of SOX4 siRNAs or a control GFP expression vector. Each transfection was performed in duplicate on two separate days. Total RNA was harvested 24 hours post-transfection

2008-11-14 | E-GEOD-11914 | biostudies-arrayexpress

SOX4 effect on LNCaP prostate cancer cells

Project description:This SuperSeries is composed of the following subset Series: GSE11874: Chromatin Immunoprecipitation microarray data from antiHA IP in stable LNCaP cells expressing either YFP or HA-SOX4/YFP GSE11913: Illumina expression data from LNCaP cells overexpressing either SOX4 or GFP GSE11914: Expression data from LNCaP cells transfected with SOX4 cDNA, SOX4 siRNA or GFP cDNA Refer to individual Series

2008-11-09 | E-GEOD-11915 | biostudies-arrayexpress

Genes regulated by SOX4 in glioblastoma cell line

Project description:Overexpression of SOX4 in LN229 glioblastoma cells prevents their cell cycle We used microarrays to detail the global programme of gene expression in SOX4 overexpression LN229 cells compared with mock control LN229 cells SOX4 overexpression LN229 cells and and control LN229 cells were cultured in DMEM cell culture media for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain the genes regulated by SOX4 in glioblastoma cell lines.

2014-09-30 | E-GEOD-51301 | biostudies-arrayexpress

Gene expression in epithelial, EMT (epithelial-mesenchymal transition) and MET (mesenchymal-epithelial transition) cells

Project description:NMuMG is an epithelial cell line that can be induced into EMT by TGF-β treatment or MET by TGF-β withdrawl. During EMT, several marker genes were downregulated/upregulated, which is consistent with its mesenchymal phenotype. Transcription factors that are regulated during EMT and its reverse process MET are candidate genes for the regulations of the EMT marker genes. NMuMG cells treated with vehicle, TGF-β for 11 days, or 11days of TGF-β treatment followed by TGF-β withdrawl for another 13 days. RNA from these 3 conditions of NMuMG were extracted and subject to microarray analysis

2013-07-26 | E-GEOD-48204 | biostudies-arrayexpress

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