Evidence map›Paper›PMID 31590360›Full record

ArticleCells2019

Acetylcholine Receptor Activation as a Modulator of Glioblastoma Invasion.

Emily G Thompson, Harald Sontheimer

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

38 citing papers in PubMed, 48 citations in OpenAlex.

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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

2 authors at 2 institutions in 1 country.

Emily G ThompsonGlial Biology in Health, Disease and Cancer Center, Fralin Biomedical Institute at Virginia Tech-Carilion, Roanoke, VA 24016, USA. egthomp@vt.edu.
Harald SontheimerGlial Biology in Health, Disease and Cancer Center, Fralin Biomedical Institute at Virginia Tech-Carilion, Roanoke, VA 24016, USA. sontheim@vt.edu.
Carilion Clinic · USUniversity of Alabama at Birmingham · US

Funding

The Role of Ion Transport in Glioma Migration, Proliferation, and ApoptosisR01NS036692 · NINDS · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI SONTHEIMER, HARALD W · 1997 to 2024
$6.8M
Amino Acid Transport and the Biology of Human GliomasR01NS052634 · NINDS · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI SONTHEIMER, HARALD W · 2005 to 2015
$3.7M
Training Program in Brain Tumor BiologyT32NS048039 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BENVENISTE, ETTY N · 2007 to 2017
$2.0M
Regulation of Amino-acid Transport in Human GliomasR01CA227149 · NCI · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI SONTHEIMER, HARALD W · 2019 to 2023
$1.8M
Glioma-Astrocyte Vascular InteractionsR01NS082851 · NINDS · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI SONTHEIMER, HARALD W · 2013 to 2016
$1.3M
NCI NIH HHS R01 CA227149NINDS NIH HHS R01 NS036692NINDS NIH HHS R01 NS052634NINDS NIH HHS R01 NS082851NINDS NIH HHS T32 NS048039
6 · The paper itself

Abstract

Grade IV astrocytomas, or glioblastomas (GBMs), are the most common malignant primary brain tumor in adults. The median GBM patient survival of 12-15 months has remained stagnant, in spite of treatment strategies, making GBMs a tremendous challenge clinically. This is at least in part due to the complex interaction of GBM cells with the brain microenvironment and their tendency to aggressively infiltrate normal brain tissue. GBMs frequently invade supratentorial brain regions that are richly innervated by neurotransmitter projections, most notably acetylcholine (ACh). Here, we asked whether ACh signaling influences the biology of GBMs. We examined the expression and function of known ACh receptors (AChRs) in large GBM datasets, as well as, human GBM cell lines and patient-derived xenograft lines. Using RNA-Seq data from the "The Cancer Genome Atlas" (TCGA), we confirmed the expression of AChRs and demonstrated the functionality of these receptors in GBM cells with time-lapse calcium imaging. AChR activation did not alter cell proliferation or migration, however, it significantly increased cell invasion through complex extracellular matrices. This was due to the enhanced activity of matrix metalloproteinase-9 (MMP-9) from GBM cells, which we found to be dependent on an intracellular calcium-dependent mechanism. Consistent with these findings, AChRs were significantly upregulated in regions of GBM infiltration in situ (Ivy Glioblastoma Atlas Project) and elevated expression of muscarinic AChR M

Indexed as

AnimalsBrain NeoplasmsCell Line, TumorDatasets as TopicGlioblastomaHumansMatrix Metalloproteinase 9MiceNeoplasm InvasivenessReceptors, CholinergicMatrix Metalloproteinase 9MMP9 protein, humanReceptors, Cholinergicacetylcholine receptorsglioblastomainvasionmatrix metalloproteinases

Identifiers

PMID31590360
PMCPMC6829263
OpenAlexW2978620939

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.