Suppressio​n of MicroRNA-9 by Mutant EGFR Signaling Induces FOXP1 to Enhance Glioblasto​ma Tumorigeni​city

ABSTRACT: 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 EG

ORGANISM(S): Homo sapiens

SUBMITTER: Frank Furnari 

PROVIDER: E-GEOD-53504 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress