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Series GSE53504 Query DataSets for GSE53504
Status Public on Dec 20, 2013
Title Suppressio​n of MicroRNA-9 by Mutant EGFR Signaling Induces FOXP1 to Enhance Glioblasto​ma Tumorigeni​city
Organism Homo sapiens
Experiment type Non-coding RNA profiling by array
Summary 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.
 
Overall design 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.
 
Citation(s) 24436148
Submission date Dec 19, 2013
Last update date Mar 21, 2014
Contact name Frank B Furnari
E-mail(s) ffurnari@ucsd.edu
Phone 858-534-7819
Organization name Ludwig Institute for Cancer Research
Lab Tumor Biology
Street address 9500 Gilman Dr.
City La Jolla
State/province CA
ZIP/Postal code 92093
Country USA
 
Platforms (1)
GPL16744 OSU-CCC Human and Mouse MicroRNA Microarray Version 4.0 [condensed human miRNA version]
Samples (36)
GSM1295001 U178 -rep1
GSM1295002 U178 -rep2
GSM1295003 U178 -rep3
Relations
BioProject PRJNA232148

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Supplementary file Size Download File type/resource
GSE53504_RAW.tar 16.4 Mb (http)(custom) TAR (of GPR)
Processed data included within Sample table

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