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Genes regulated by Sox2 in glioma cancer cell line

ABSTRACT: Knockdown of Sox2 in LN229 gliomal cancer cells decrease their growth rates in vitro. We used microarrays to detail the global programme of gene expression in Sox2 Knockdown LN229 cells compared with mock knockdown LN229 cells Sox2 knockdown LN229 cells and and mock knockdown LN229 cells were cultured in DMEM cell culture media for RNA extraction and hybridization on Applied Biosystems Human Genome Survey Microarrays . We sought to obtain the genes regulated by Sox2 in glioma cell line.

ORGANISM(S): Homo sapiens

SUBMITTER: Biao Yang Lin

PROVIDER: E-GEOD-23838 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The SOX2 response program in glioblastoma multiforme: an integrated ChIP-seq, expression microarray, and microRNA analysis.

Fang Xuefeng X Yoon Jae-Geun JG Li Lisha L Yu Wei W Shao Jiaofang J Hua Dasong D Zheng Shu S Hood Leroy L Goodlett David R DR Foltz Gregory G Lin Biaoyang B

BMC genomics 20110106

<h4>Background</h4>SOX2 is a key gene implicated in maintaining the stemness of embryonic and adult stem cells. SOX2 appears to re-activate in several human cancers including glioblastoma multiforme (GBM), however, the detailed response program of SOX2 in GBM has not yet been defined.<h4>Results</h4>We show that knockdown of the SOX2 gene in LN229 GBM cells reduces cell proliferation and colony formation. We then comprehensively characterize the SOX2 response program by an integrated analysis us ...[more]

PMID: 21211035

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An integrative analysis of the SOX2 response program in glioblastoma

Project description:This SuperSeries is composed of the following subset Series: GSE23795: Chip-Seq analysis of Sox2 protein genome-wide DNA binding sites in glioma cancer cells GSE23838: Genes regulated by Sox2 in glioma cancer cell line Refer to individual Series

2011-01-10 | E-GEOD-23839 | biostudies-arrayexpress

Genes regulated by Sox2 in glioma cancer cell line

Project description:Knockdown of Sox2 in LN229 gliomal cancer cells decrease their growth rates in vitro. We used microarrays to detail the global programme of gene expression in Sox2 Knockdown LN229 cells compared with mock knockdown LN229 cells

2011-01-10 | GSE23838 | GEO

Genes regulated by Sox2 in colorectal cancer cell line

Project description:Knockdown of Sox2 in SW620 colorectal cancer cells decrease their growth rates in vitro and in vivo in xenograft models. We used microarrays to detail the global programme of gene expression in Sox2 Knockdown sw620 cells compared with mock knockdown sw620 cells Sox2 knockdown sw620 cells and and mock knockdown sw620 cells were cultured in RPMI 1640 cell culture media for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain the genes regulated by Sox2 in colorectal cell lines and end (T4) of gastrulation.

2011-03-01 | E-GEOD-20689 | biostudies-arrayexpress

Modulation of gene expression in U251 glioblastoma cells by binding of mutant p53 to intronic and intergenic sequences

Project description:Missense point mutations in the TP53 gene are frequent genetic alterations in human tumor tissue and cell lines derived thereof. Mutant p53 (mutp53) proteins have lost sequence-specific DNA binding, but have retained the ability to interact in a structure-selective manner with non-B DNA and to act as regulators of transcription. To identify functional binding sites of mutp53, we established a small library of genomic sequences bound by p53R273H in U251 human glioblastoma cells using chromatin immunoprecipitation (ChIP). Mutp53 binding to isolated DNA fragments confirmed the specificity of the ChIP. The mutp53 bound DNA sequences are rich in repetitive DNA elements, which are dispersed over non-coding DNA regions. Stable down-regulation of mutp53 expression strongly suggested that mutp53 binding to genomic DNA is functional. We identified the PPARGC1A and FRMD5 genes as p53R273H targets regulated by binding to intronic and intra-genic sequences. We propose a model that attributes the oncogenic functions of mutp53 to its ability to interact with intronic and intergenic non-B DNA sequences and modulate gene transcription via re-organization of chromatin. For the study of the consequences of mutant p53 (R273H) knockdown on gene expression, total RNA from parental U251 glioblastoma cells and UsiA12 clone was prepared from two independent cell culture experiments (biological replicates) and processed for microarray-based profiling of gene expression. UsiA12 clone was derived from the U251 cells transfected with the pSuper-p53 and pCI-neo vectors.

2010-06-24 | E-GEOD-13991 | biostudies-arrayexpress

Progerin Expression in Endothelial Cells Induces Endothelial Dysfunction

Project description:Hutchinson-Gilford Progeria Syndrome (HGPS) is a rare, genetic premature aging disorder associated with severe atherosclerosis, often resulting in fatal heart attacks and strokes. Progerin, the mutant protein in HGPS, also is expressed in healthy individuals and may play a role in the development of atherosclerosis during physiologic aging. Here, we provide evidence for a primary involvement of vascular endothelium in the pathogenesis of accelerated atherosclerosis in HGPS. Expression of progerin in cultured human endothelial cells induces a dysfunctional phenotype, manifested by activation of multiple pro-inflammatory, pro-atherogenic genes. In particular, our data implicate endothelial-derived interleukin-1 (IL-1) as a key mediator of a pro-inflammatory vascular phenotype. Endothelial activation also is detectable in a mouse model of HGPS, and appears to be conveyed to neighboring vascular cells via autocrine and paracrine signaling. These new mechanistic insights into the vascular pathobiology of HGPS may have therapeutic implications for this disease. Genome-wide transcriptional profiling was carried out to assess functional phenotypic changes in endothelial cells (EC) as a result of progerin expression. Cultured EC were infected with an adenovirus expressing progerin (Ad-Progerin), and as a control, an adenovirus that did not express any construct (Ad-Null). Experiments were preformed with three different EC cultures.

2010-12-02 | E-GEOD-19270 | 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

2014-09-30 | GSE51301 | GEO

Placental gene expression in severe preeclampsia.

Project description:The series is composed of thirty hybridizations for analysis of differentially expressed genes in normal placenta tissues from patients with normal labor and placenta tissues from patients with severe preeclampsia. Patients tissues samples were obtained from (Vasilis. Total RNA extraction was performed by using the MagNa Pure Compact RNA Isolation Kit (Roche Applied Science). Keywords: Gene expression study, Disease state Twenty-six out of 50 normal placentas were randomly selected to match with 17 preeclamptic placentas, accounting for parity. Microarrays were performed applying a direct comparison design.

2010-05-26 | E-GEOD-10588 | biostudies-arrayexpress

Genes regulated by miR-127-3p in glioblastoma cell line

Project description:Overexpression of miR-127-3p in LN229 glioblastoma cells promotes their migration and invasion in vitro and in vivo in xenograft models. We used microarrays to detail the global programme of gene expression in miR-127-3p overexpression LN229 cells compared with mock overexpression LN229 cells

2014-09-01 | GSE50173 | GEO

TAF6 orchestrates transcription programs and apoptosis in the absence of p53

Project description:The decision of metazoan cells to live or undergo programmed cell death hinges on the balance between the levels of pro- versus anti-apoptotic gene products. The general RNA polymerase II (Pol II) transcription factor, TFIID, plays a central role in the regulation of gene expression through its core promoter recognition and co-activator functions. The core TFIID subunit TAF6 is a co-activator for the pro-apoptotic p53 tumour suppressor protein. Our previous studies identified a specialized isoform of TAF6, termed TAF6 that can specifically be induced in apoptosis. To elucidate the impact of TAF6 on gene expression and cell death, we employed modified antisense oligonucleotides to enforce expression of endogenous TAF6. The induction of endogenous TAF6 triggered apoptosis in several cancer cell lines. Importantly, TAF6 also induces apoptosis in tumor cell lines devoid of p53, placing TAF6 function downstream of p53. Microarray experiments uncovered a TAF6-induced transcriptome landscape displaying enhanced expression of genes of the Notch, oxidative stress, integrin, p53 and apoptosis pathways. Our data show that the TAF6 pathway is a pivotal signalling nexus that controls pro-apoptotic gene expression programs. Keywords: Treatment with splice site switching antisense oligonucleotides, induction of apoptosis Biological triplicates, 3 conditions: control oligonucleotide, Taf6 oligonucleotide, specificity control Bcl-x oligonucleotide

2010-11-27 | E-GEOD-8752 | biostudies-arrayexpress

Determining the impact of alternative splicing events on transcriptome dynamics

Project description:Background The complete sequencing of the human genome and its subsequent analysis revealed a predominant role for alternative splicing in the generation of proteome diversity. Splice switching oligonucleotides (SSOs) are a powerful and specific tool to experimentally control alternative splicing of endogenous messenger RNAs in living cells. SSOs also have therapeutic potential to treat diseases that are caused by aberrant splicing. The assignment of biological roles to alternative splicing events of currently unknown function promises to provide a largely untapped source of potential new therapeutic targets. Here we have developed a protocol that combines high sensitivity microarrays with the transfection of SSOs to monitor global changes in gene expression downstream of alternate, endogenous splice events. Findings When applied to a well-characterized splicing event in the Bcl-x gene, the application of high sensitivity microarrays revealed a link between the induction of the Bcl-xS isoform and the repression of genes involved in protein synthesis. Conclusions The strategy introduced herein provides a useful approach to define the biological impact of any given alternative splicing event on global gene expression patterns. Furthermore, our data provide the first link between Bcl-xS expression and the repression of ribosomal protein gene expression. Biological triplicates, 2 conditions: control oligonucleotide, Bcl-x oligonucleotide

2008-10-02 | E-GEOD-9851 | biostudies-arrayexpress

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