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SOX4 effect on LNCaP prostate cancer cells

ABSTRACT: 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

ORGANISM(S): Homo sapiens

SUBMITTER: Chris Scharer

PROVIDER: E-GEOD-11915 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide promoter analysis of the SOX4 transcriptional network in prostate cancer cells.

Scharer Christopher D CD McCabe Colleen D CD Ali-Seyed Mohamed M Berger Michael F MF Bulyk Martha L ML Moreno Carlos S CS

Cancer research 20090101 2

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 exact role of SOX4 in cancer progression is not well understood. Here, we have identified the direct transcriptional targets of SOX4 using a combination of genome-wide localization chromatin immunoprecipitation-chip analysis and transient overexpression followed by expression ...[more]

PMID: 19147588

Similar Datasets

Chromatin Immunoprecipitation microarray data from antiHA IP in stable LNCaP cells expressing either YFP or HA-SOX4/YFP

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 identified the direct transcriptional targets of SOX4 using a genome-wide localization ChIP-chip analysis. Keywords: ChIP-chip LNCaP prostate cancer cells were stably infected with a lentivirus containing either HA-SOX4-IRES-YFP or IRES-YFP alone. Cells were sorted for YFP expression and expanded in tissue culture before chromatin immunoprecipitation against the HA epitope tag was performed.

2008-11-09 | E-GEOD-11874 | biostudies-arrayexpress

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

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

SOX4 genome binding targets in glioblastoma cell line

Project description:Overexpression of SOX4 in LN229 glioblastoma cells prevents their cell cycle Examination of SOX4 binding profile in prostate cell LN229-SOX4 with LN229-GFP as negative control.

2014-10-20 | E-GEOD-51663 | biostudies-arrayexpress

SOX4 supports cancer stemness by enhancing HDAC1 transcription revealed by comparative proteomics

Project description:We have investigated the proteome changes induced by SOX4 overexpression in HCT-116 cells using iTRAQ-based quantitative proteomics. Bioinformatics analysis revealed that HDAC1 could be one of the important regulators in cancer stem cells (CSCs) maintenance. We found that SOX4 transcriptionally regulates HDAC1 to support the stemness of cancer stem cells (CSCs). This work revealed a novel underlying mechanism, SOX4-HDAC1 axis, for stemness maintenance of human cancer.

2021-09-09 | PXD019694 | Pride

Gene expression of LNCaP human prostate cells by cholesterol diet

Project description:Understanding the systemic regulation of normal prostate gene expression by cholesterol diet is critical for deciphering the mechanisms responsible for the transition from healthy to pathogenic prostate conditions. To understand mechanism under cholesterol effect on prostate, we performed microarray analysis using LNCaP human prostate cells cultured in low cholesterol medium. The RNA is obtained from LNCaP human prostate cells serum-starved for 0h, 3h, 16h followed by CLM medium.

2011-12-01 | E-GEOD-25472 | 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

SOX4 AND SMARCA4 COOPERATIVELY REGULATE PI3K SIGNALING THROUGH TRANSCRIPTIONAL ACTIVATION OF TGFBR2 IN BASAL LIKE BREAST CANCER

2021-03-02 | PXD022811 | Pride

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

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

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