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The target genes of EGFR activity in glioma cells

ABSTRACT: As a first step towards identifying the target genes of EGFR activity in glioma cells, genome-wide expression analyses were performed using the Affymetrix GeneChip Human Genome U133A array. To accomplish this, mRNA expression levels of these genes were measured in the glioblastoma cell lines, U87 and U178, engineered with EGFR by retrovirus transduction (termed U87-EGFR and U178-EGFR respectively), with or without 20 ng/mL EGF treatment for 3 h.

ORGANISM(S): Homo sapiens

PROVIDER: GSE33442 | GEO | 2011/11/05

SECONDARY ACCESSION(S): PRJNA148697

REPOSITORIES: GEO

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The target genes of EGFR activity in glioma cells

Project description:As a first step towards identifying the target genes of EGFR activity in glioma cells, genome-wide expression analyses were performed using the Affymetrix GeneChip Human Genome U133A array. To accomplish this, mRNA expression levels of these genes were measured in the glioblastoma cell lines, U87 and U178, engineered with EGFR by retrovirus transduction (termed U87-EGFR and U178-EGFR respectively), with or without 20 ng/mL EGF treatment for 3 h. U87 and U178 cells engineered to express EGFR were stimulated with or without EGF. The experiment was replicated twice for each U87 and U178 cells.

2011-11-05 | E-GEOD-33442 | biostudies-arrayexpress

Suppression of MicroRNA-9 by Mutant EGFR Signaling Induces FOXP1 to Enhance Glioblastoma Tumorigenicity

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

RNA-seq Analysis of U87: Ctrl, U87:EGFR, U87:EGFRvIII, U87:EGFR+EGFRvIII and U87:EGFR+EGFRvIII KRAS KO

Project description:RNA-seq Analysis of U87: Ctrl, U87:EGFR, U87:EGFRvIII, U87:EGFR+EGFRvIII and U87:EGFR+EGFRvIII KRAS KO

| PRJNA483397 | ENA

Tumor-associated monocytes promote mesenchymal transformation through EGFR signaling in glioma

Project description:The role of brain immune compartments in glioma evolution remains elusive. We profiled immune cells in glioma microenvironment and the matched peripheral blood from 11 patients at a single-cell level. Notably, glioblastoma exhibits specific infiltration of certain blood-originated monocytes expressing EGFR ligands including EREG and AREG, coined as tumor-associated monocytes (TAMo). TAMo infiltration is mutually exclusive with EGFR alterations (P = 0.019), while co-occurring with mesenchymal subtype (P = 4.7x10-7) and marking worse prognosis (P = 0.004 and 0.032 in two independent cohorts). Evolutionary analysis of initial-recurrent glioma pairs and single-cell study of a multi-centric glioblastoma reveals remarkable association between elevated TAMo and glioma mesenchymal transformation. Further analysis identifies FOSL2 as a master regulator of TAMo. The roles of FOSL2-EREG/AREG-EGFR signaling axis in promoting glioma invasion were verified experimentally. Collectively, we have identified TAMo in tumor microenvironment and revealed its driving role in activating EGFR signaling to shape glioma evolution.

2023-08-01 | GSE237779 | GEO

Analysis of phospho-tyrosine signaling after glucose starvation

Project description:U87-EGFRvIII GBM cells treated with EGF (10 ng/ml, 5 min)

2012-06-25 | PRD000593 | Pride

FAT1 knockdown in immortalized astrocyte and glioma cell lines

Project description:The FAT1 gene was knocked down using 2 independent siRNAs, in immortalized human astrocytes and U87 and U251 glioma cell lines. A non-targeted scramble siRNA was used as a control. Scramble, FAT1 siRNA#1 and FAT1 siRNA#2 were transfected into each cell line, in duplicate, and RNA analyzed using the Affymetrix U133A 2.0 platform.

2013-01-10 | E-GEOD-40583 | biostudies-arrayexpress

EGFR/FOXO3a/BIM signalling pathway determines chemosensitivity of BMP4-differentiated glioma stem cells to temozolomide

Project description:Accumulating evidence suggests that glioma stem cells (GSCs), rare cells characterised by pluripotency and self-renewal, are responsible for glioblastoma (GBM) propagation, recurrence and resistance to therapy. Differentiation with bone morphogenic proteins (BMPs) is considered to be a promising approach to eliminate GSCs and sensitise glioma to chemotherapeutics. Epidermal growth factor receptor (EGFR) gene alterations are detected in more than a half of GBMs, however, the role of EGFR in chemoresistance of glioma stem cells remain elusive. Here, we investigated whether EGFR signalling affects BMP4-induced differentiation of GSCs and their response to an alkylating drug temozolomide (TMZ). We show that BMP4 triggers Smad signalling cascade in glioma stem cells independently of the EGFR level. BMP4 down-regulated levels of pluripotency markers (SOX2 and OLIG2) with the concomitant induction of astrocytic (GFAP) and neuronal (b-Tubulin III) markers. However, significant differences in chemotherapy outcomes were observed in glioma stem cells with different EGFR levels. BMP4-induced differentiation did not enhance sensitivity to TMZ in EGFRlow GSCs, in contrast to EGFRhigh GSCs, which were undergoing apoptosis. We identified differences in cell cycle regulation by analyses of cell cycle phase distribution and cell-cycle-related proteins. In cells with lower EGFR expression BMP4 triggered the G1 cell cycle arrest, not detected in EGFRhigh cells. RNA-seq profiles further highlighted transcriptomic alternations and distinct processes characterizing EGFR-dependent responses in course of BMP4-induced differentiation. We identified AKT/FOXO3a axis controlling of BIM (the pro-apoptotic BCL-2 family protein) as operating only in EGFRhigh BMP4-differentiated and TMZ-treated cells.

2021-05-05 | GSE140441 | GEO

Expression data from U87 glioma cells and U87-2M1 glioma cells

Project description:An experimental lung metastasis assay was used to derive an invasive subline of U87 that is metastatic in mice. We used microarray analyses to find out over-represented gene ontologies that can explain the observed enhanced invasiveness of U87-2M1 cells. Early passage U87-2M1 cells and parental U87 glioma cells from ATCC were selected for RNA extraction and hybridization on microarray

2012-12-31 | E-GEOD-35169 | biostudies-arrayexpress

Expression comparison of mutant EGFR-driven gliomas with relapse tumors upon mutant EGFR ablation

Project description:To determine the roles of oncogenic EGFR signaling in gliomagenesis and tumor maintenance, we generated a novel glioma mouse model driven by inducible expression of a mutant EGFR (EGFR*). Genetic suppression of EGFR* induction led to significant tumor regression and prolonged survival. But in spite of the initial response, the tumors relapsed invariably and propagated independent of EGFR*. We used microarrys to directly compare geen expression of control and relapse tumors and identified gene sets specifically activated in relapse tumors. Control and relasped glioma samples upon mutant EGFR extinction were selected for RNA extraction and hybridization on Affymetrix microarrays.

2015-01-08 | E-GEOD-64751 | biostudies-arrayexpress

RNA-seq Analysis of U87: Ctrl, U87:EGFR, U87:EGFRvIII, U87:EGFR+EGFRvIII and U87:EGFR+EGFRvIII KRAS KO

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

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