Expression data from human GBMs
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE51062 | GEO | 2015/09/08
SECONDARY ACCESSION(S): PRJNA219949
REPOSITORIES: GEO
Similar Datasets
Project description:Analysis of human glioblastoma multiforme tumors revealed genes that are upregulated in tumors expressing EGFRvIII compared to those expressing wild-type EGFR We examined gene expression in 52 primary GBM tumors, which were stratified based on the presence or absence of EGFRvIII expression using EGFRvIII-specific RT-PCR (Tykocinski et al., 2012). The extracted RNA samples from these tumors were subjected to microarray analysis using HG-U133 2.0 Plus Affymetrix gene chips. Average expression of all transcripts were compared between EGFRvIII-positive and -negative GBMs.
2015-09-08 | E-GEOD-51062 | biostudies-arrayexpress
Project description:EGFRvIII is the most common deletion mutant of EGFR in human cancer and its levels are highly correlated with poor prognosis in GBM. The deletion of exons 2-7 removes most of the extracellular ligand binding domain, so it is unable to bind EGF or other EGFR-binding ligands. Nevertheless, the mutant receptor is constitutively phosphorylated, and is capable of activating downstream signaling pathways at a low level. To comprehensively identify the downstream signaling consequences of the EGFRvIII, we incorporated phosphoproteomic, transcription profiling and DNase-Seq data from U87MG glioblastoma cells expressing titrated levels of this mutant receptor. Total RNA were extracted from U87MG cells engineered to expressed different levels of EGFRvIII: medium (U87M; 1.5 million copies of EGFRvIII receptor per cell), high (U87H; 2 million copies per cell), super-high (U87SH; 2.5 million copies per cell), and kinase-dead EGFRvIII (U87DK; 2 million copies of kinase dead EGFRvIII per cell). RNA was hybridized to Affymetrix microarrays.
2013-01-01 | E-GEOD-36901 | biostudies-arrayexpress
Project description:Glioblastoma multiforme (GBM) is a highly aggressive and heterogeneous form of primary brain tumors, driven by a complex repertoire of oncogenic alterations, including the constitutively active epidermal growth factor receptor (EGFRvIII). EGFRvIII impacts both cell-intrinsic and non-cell autonomous aspects of GBM progression, including cell invasion, angiogenesis and modulation of the tumor microenvoiront, this is, at least in part, attributable to the release and intercellular trafficking of extracellular vesicles (EVs), heterogeneous membrane structures containing multiple bioactive macromolecules. Here we analyzed the impact of EGFRvIII on the profile of glioma EVs using a series of isogenic tumor cell lines, in which this oncogene exhibits a strong transforming activity. Thus, we observed that EGFRvIII expression alters several properties of glioma EVs, including their output and global protein composition. Using mass spectrometry, quantitative proteomic analysis and Gene Ontology terms filters, we observed that EVs released by EGFRVIII-transformed cells were enriched for extracellular exosome and focal adhesion related proteins. Among them, we validated the association of pro-invasive proteins (CD44, BSG, CD151) with EVs of EGFRvIII expressing cells, and down-regulation of exosomal markers (CD81 and CD82) in EVs of their indolent counterparts. Nano-flow cytometry revealed that the EV output from individual glioma cell lines was highly heterogeneous, such that only a fraction of EVs contained specific proteins such as EGFR, CD9, or others. Notably, cells expressing EGFRvIII released ample EVs double positive for CD44/BSG, and these proteins also co-localized in cellular filopodia. We also detected the expression of homophilic adhesion molecules and increased homologous EV uptake by EGFRvIII-positive glioma cells. These results suggest that oncogenic EGFRvIII reprograms the proteome of GBM-related EVs, a notion with considerable implications for their biological activity and properties relevant for development of EV-based cancer biomarkers.
2018-07-30 | PXD008311 | Pride
Project description:We present a computational method for building a regulatory network from global phosphoproteomic and transcription profiling data. To recover the critical missing links between signaling events and transcriptional responses, we relate changes in chromatin accessibility to changes in expression and then uses these links to connect proteomic and transcriptome data. We applied our approach to integrate epigenomic, phosphoproteomic and transcriptome changes induced by the variant III mutation of the epidermal growth factor receptor (EGFRvIII) in a cell line model of glioblastoma multiforme (GBM). Genome-wide DNase I hypersensitivity followed by sequencing (DNase-Seq) to measure chromatin accessibility in a cell line derived from the U87MG glioblastoma cell line to express high level of EGFRvIII (U87H; 2 million copies of EGFRvIII per cell) and a control cell line expressing kinase dead EGFRvIII (U87DK; 2 million kinase dead EGFRvIII per cell). A prediction from the computational method, the transcriptional co-regulator p300, was experimentally validated by chromatin immunoprecipitation followed by sequencing (ChIP-Seq).
2013-01-01 | E-GEOD-36900 | biostudies-arrayexpress
Project description:To investigate the function of TLR2 in EGFR and EGFRvIII co-expressing glioblastoma cells, we knocked out TLR2 by CRISPR.
2024-08-29 | GSE212325 | GEO
Project description:Analysis of rat tumor xenografts revealed genes that are upregulated in tumors expressing EGFRvIII 12 rats received intracranial injections of 9L cells expressing EGFRvIII or an empty vector control. Three weeks after implantation and subsequent growth, tumors were aseptically removed, processed for RNA extraction, and analyzed for gene expression profiling using the RatRef12 Illumina chip array. We compared the average expression of all the transcripts between EGFRvIII-expressing and empty vector control tumors.
2015-09-08 | E-GEOD-51147 | biostudies-arrayexpress
Project description:EGFRvIII is the most common deletion mutant of EGFR in human cancer and its levels are highly correlated with poor prognosis in GBM. The deletion of exons 2-7 removes most of the extracellular ligand binding domain, so it is unable to bind EGF or other EGFR-binding ligands. Nevertheless, the mutant receptor is constitutively phosphorylated, and is capable of activating downstream signaling pathways at a low level. To comprehensively identify the downstream signaling consequences of the EGFRvIII, we incorporated phosphoproteomic, transcription profiling and DNase-Seq data from U87MG glioblastoma cells expressing titrated levels of this mutant receptor.
2013-01-01 | GSE36901 | GEO
Project description:The EGF-receptor (EGFR) is amplified and mutated in glioblastoma (GBM) where its common mutation, (∆EGFR, also called EGFRvIII) has a variety of activities that promote growth and inhibit death, thereby conferring a strong tumor-enhancing effect. This range of activities suggested to us that ∆EGFR might exert its influence through pleiotropic effectors and we hypothesized that microRNAs (miRs) might serve such a function. To test this, we determined the miR profiles of GBM cells with activated wild type EGFR (wtEGFR) and mutant EGFR (∆EGFR) to cells with non-activated EGFR or kinase dead ∆EGFR. To identify miRs regulated by EGFR, RNA from 2 different glioma cell lines (U87 and U373) were hybridized to miR expression arrays and analyzed. Each cell type was engineered to express wild type EGFR (wtEGFR), dead kinase ∆EGFR (DK) or ∆EGFR at elevated levels similar to those observed in primary glioblastomas displaying EGFR overexpression. Parental cells expressing endogenous EGFR and wtEGFR cells stimulated with EGF for 1hr were also included in the analyses.
2013-12-20 | E-GEOD-53504 | biostudies-arrayexpress
Project description:Analysis of rat tumor xenografts revealed genes that are upregulated in tumors expressing EGFRvIII
2015-09-08 | GSE51147 | GEO
Project description:We found that U87 cells expressing EGFR and EGFRvIII upregulated a large group of cytokines. The upregulation of many of these cytokines was dependent on KRAS.
2018-11-01 | GSE117838 | GEO