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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. 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Frank Furnari

PROVIDER: E-GEOD-33442 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

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

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Project description:The Epidermal Growth Factor Receptor (EGFR) has been studied extensively due to its critical role in cellular signaling and association with disease. Previous models have elucidated interactions between EGFR and downstream adaptor proteins, or showed phenotypes affected by EGFR. However, the link between EGFR phosphorylation and phenotypic outcome is still poorly understood. Here, we employed a suite of isogenic cells lines expressing site-specific mutations at each of the EGFR C-terminal phosphorylation sites to interrogate their role in signaling network and cell biological response to stimulation. Our results demonstrate the resilience of the EGFR network, which was largely similar even in the context of multiple Y-to-F mutations in the EGFR C-terminal tail, while also revealing nodes in the network that have not previously been linked to EGFR signaling. Our data-driven model highlights signaling network nodes associated with distinct EGF-driven cell responses, including migration, proliferation, and receptor trafficking. Application of this same approach to less studied RTKs should provide a plethora of novel associations that should lead to a much better understanding of these signaling networks.

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