Evidence map›Paper›PMID 29318454›Full record

ArticleMolecular and cellular biochemistry2018

GL261 glioma tumor cells respond to ATP with an intracellular calcium rise and glutamate release.

Averey D Strong, M Caitlin Indart, Nolan R Hill, Richard L Daniels

Abstract read
In one paragraph

Article in Molecular and cellular biochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 24 citations in OpenAlex.

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  16. The P2X7 Receptor: Central Hub of Brain Diseases.Frontiers in molecular neuroscience · 2020
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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

4 authors at 1 institution in 1 country.

Averey D StrongDepartment of Biology, The College of Idaho, Caldwell, ID, 83605, USA.
M Caitlin IndartDepartment of Biology, The College of Idaho, Caldwell, ID, 83605, USA.
Nolan R HillDepartment of Biology, The College of Idaho, Caldwell, ID, 83605, USA.
Richard L DanielsDepartment of Biology, The College of Idaho, Caldwell, ID, 83605, USA. Ldaniels@collegeofidaho.edu.ORCID http://orcid.org/0000-0003-2477-6025
College of Idaho · US

Funding

Women's health: interplay of maternal diet and key demographics on neurological health in the rural frontier and remote WestP20GM103408 · NIGMS · UNIVERSITY OF IDAHO · PI Carolyn Hovde Bohach · 2012 to 2026
$59.8M
M.J. Murdock Charitable Trust Research Startup Grant for new Science FacultyMountain State Tumor Institute Small Projects GrantMountain State Tumor Institute Summer Fellows ProgramNational Institute of General Medical Sciences P20GM103408NIGMS NIH HHS P20 GM103408
6 · The paper itself

Abstract

Glioblastoma (GBM) is an aggressive brain cancer with an average survival rate of 15 months. The composition of the GBM tumor microenvironment-its pH, the presence of growth and immune factors, neurotransmitters, and gliotransmitters-plays an important role in GBM pathophysiology and facilitates tumor survival and growth. In particular, GBM tumor cells produce glutamate, which is toxic to healthy tissue and is associated with increased tumor invasion into adjacent brain regions. The conditions that lead to this excitotoxic release of glutamate are not completely understood. Previous studies have demonstrated that extracellular ATP is present at high levels in the tumor microenvironment, and that ATP stimulates the release of glutamate from astrocytes in culture. Here we examine the functional effects of extracellular ATP on the GL261 cell line, a model system for high-grade astrocytomas such as GBM. We show that treatment with ATP leads to an immediate, dose-dependent influx of calcium into the cell that is partially inhibited by an antagonist (o-ATP) of the ionotropic ATP receptor P2X7. In addition, GL261 cells respond to extracellular ATP with a dose-dependent release of glutamate. Consistent with other reports, we find that ATP is toxic to GL261 cells at high concentrations. Together, these results provide insight into the mechanisms responsible for glutamate production by tumor cells and inform future studies that will identify how the GBM tumor microenvironment facilitates tumor invasion into healthy areas of the brain.

Indexed as

Adenosine TriphosphateCalciumCalcium SignalingCell Line, TumorGliomaGlutamic AcidHumansNeoplasm ProteinsReceptors, Purinergic P2X7Tumor MicroenvironmentAdenosine TriphosphateCalciumGlutamic AcidNeoplasm ProteinsReceptors, Purinergic P2X7ATPCalcium imagingGL261GlioblastomaGlutamateMTTTumor microenvironment

Identifiers

PMID29318454
PMCPMC6037622
OpenAlexW2783049130

What OpenQuestion holds

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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.