NDLI: Glutamate promotes cell growth by EGFR signaling on U-87MG human glioblastoma cell line.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Schunemann, Daniel Pretto Grivicich, Ivana Regner, Andréa Leal, Lisiane Freitas de Araújo, Daniela Romani Jotz, Geraldo Pereira Fedrigo, Carlos Alexandre Simon, Daniel da Rocha, Adriana Brondani
Description	Country affiliation: Brazil Author Affiliation: Schunemann DP ( Laboratório de Marcadores de Estresse Celular, Centro de Pesquisas em Ciências Médicas, Universidade Luterana do Brasil, Canoas, RS, Brazil.)
Abstract	Accumulating evidences suggest that glutamate plays a key role in the proliferation and invasion of malignant glioblastoma (GBM) tumors. It has been shown that GBM cells release and exploit glutamate for proliferation and invasion through AMPA glutamate receptors. Additionally, amplification of the epidermal growth factor receptor (EGFR) gene occurs in 40-50% of GBM. Since, PI3K/Akt is considered one of the main intracellular pathways involved in EGFR activation, AKT functions could trigger EGFR signaling. Thus, we investigated whether EGFR-phospho-Akt pathway is involved on the glutamate inducing U-87MG human GBM cell line proliferation. For these purpose, we treated the U-87MG cell line with 5 to 200 mM of glutamate and assessed the number of viable cells by trypan blue dye exclusion test. An increase in cell number (50%) was found at 5 mM glutamate, while the addition of DNQX (500 microM), an antagonist of AMPA receptor, inhibited the effect of glutamate on the U87-MG cells proliferation. Also, at 5 mM glutamate we observed an increase on the EGFR and phospho-Akt contents evaluated by immunohistochemistry. Moreover, U-87MG cells treated with glutamate exhibited an increase about 2 times in the EGFR mRNA expression. While, in the presence of the anti-EGFR gefitinib (50 muM) or the PI3K inhibitor wortmannin (5 muM), the U-87MG proliferation was restored to control levels. Together, our data suggest that glutamate signaling mediated by AMPA receptor induces U-87MG human GBM cell line proliferation via EGFR-phospho-Akt pathway.
File Format	HTM / HTML
ISSN	12194956
Issue Number	2
Volume Number	16
e-ISSN	15322807
Journal	Pathology & Oncology Research
Language	English
Publisher	Springer
Publisher Date	2010-06-01
Publisher Place	Netherlands
Access Restriction	Subscribed
Subject Keyword	Discipline Oncology Cell Proliferation Drug Effects Glioblastoma Metabolism Glutamic Acid Receptor, Epidermal Growth Factor Cell Line, Tumor Humans Image Processing, Computer-assisted Immunohistochemistry Proto-oncogene Proteins C-akt Receptors, Ampa Reverse Transcriptase Polymerase Chain Reaction Signal Transduction Physiology Journal Article
Content Type	Text
Resource Type	Article
Subject	Cancer Research Pathology and Forensic Medicine Oncology

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