Evidence map›Paper›PMID 19997873›Full record

ArticlePathology oncology research : POR2010

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

Daniel Pretto Schunemann, Ivana Grivicich, Andréa Regner, Lisiane Freitas Leal, Daniela Romani de Araújo, Geraldo Pereira Jotz, Carlos Alexandre Fedrigo, Daniel Simon, Adriana Brondani da Rocha

Abstract read
PubMed Publisher
In one paragraph

Article in Pathology oncology research : POR, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.1field-weighted citation impact, top 24% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. The Role of Hyperexcitability in Gliomagenesis.International journal of molecular sciences · 2023
    Review
  9. Article
  10. Article
  11. Review
  12. Activation of Dopamine Receptor 2 Prompts Transcriptomic and Metabolic Plasticity in Glioblastoma.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  13. Aberrant receptor tyrosine kinase signaling in lipofibromatosis: a clinicopathological and molecular genetic study of 20 cases.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2019
    Article
  14. Review
  15. Article
  16. A pathway map of glutamate metabolism.Journal of cell communication and signaling · 2016
    Article
  17. Glutamate prevents intestinal atrophy via luminal nutrient sensing in a mouse model of total parenteral nutrition.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014
    Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Daniel Pretto SchunemannLaboratório de Marcadores de Estresse Celular, Centro de Pesquisas em Ciências Médicas, Universidade Luterana do Brasil, Canoas, RS, Brazil.
Ivana Grivicich
Andréa Regner
Lisiane Freitas Leal
Daniela Romani de Araújo
Geraldo Pereira Jotz
Carlos Alexandre Fedrigo
Daniel Simon
Adriana Brondani da Rocha
Universidade Luterana do Brasil · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Cell Line, TumorCell ProliferationErbB ReceptorsGlioblastomaGlutamic AcidHumansImage Processing, Computer-AssistedImmunohistochemistryProto-Oncogene Proteins c-aktReceptors, AMPAReverse Transcriptase Polymerase Chain ReactionSignal TransductionErbB ReceptorsGlutamic AcidProto-Oncogene Proteins c-aktReceptors, AMPA

Identifiers

PMID19997873
OpenAlexW2044509093

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.