Evidence map›Paper›PMID 30291908›Full record

ReviewPharmacology & therapeutics2019

Acetylcholine signaling system in progression of lung cancers.

Jamie R Friedman, Stephen D Richbart, Justin C Merritt, Kathleen C Brown, Nicholas A Nolan, Austin T Akers, Jamie K Lau, Zachary R Robateau, Sarah L Miles, Piyali Dasgupta

Open access · greenAbstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

77 citing papers in PubMed, 117 citations in OpenAlex.

  1. The Role of the Nervous System in Lung Disease.Current neurology and neuroscience reports · 2026
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17 more citing papers are in PubMed but not listed here.

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

10 authors at 2 institutions in 1 country.

Jamie R FriedmanDepartment of Biomedical Sciences, Joan C. Edwards School of Medicine, 1700 Third Avenue, Huntington, WV 25755.
Stephen D RichbartDepartment of Biomedical Sciences, Joan C. Edwards School of Medicine, 1700 Third Avenue, Huntington, WV 25755.
Justin C MerrittDepartment of Biomedical Sciences, Joan C. Edwards School of Medicine, 1700 Third Avenue, Huntington, WV 25755.
Kathleen C BrownDepartment of Biomedical Sciences, Joan C. Edwards School of Medicine, 1700 Third Avenue, Huntington, WV 25755.
Nicholas A NolanDepartment of Biomedical Sciences, Joan C. Edwards School of Medicine, 1700 Third Avenue, Huntington, WV 25755.
Austin T AkersDepartment of Biomedical Sciences, Joan C. Edwards School of Medicine, 1700 Third Avenue, Huntington, WV 25755.
Jamie K LauBiology Department, Center for the Sciences, Box 6931, Radford University, Radford, Virginia 24142.
Zachary R RobateauDepartment of Biomedical Sciences, Joan C. Edwards School of Medicine, 1700 Third Avenue, Huntington, WV 25755.
Sarah L MilesDepartment of Biomedical Sciences, Joan C. Edwards School of Medicine, 1700 Third Avenue, Huntington, WV 25755.
Piyali DasguptaDepartment of Biomedical Sciences, Joan C. Edwards School of Medicine, 1700 Third Avenue, Huntington, WV 25755. Electronic address: dasgupta@marshall.edu.
Marshall University · USRadford University · US

Funding

Capsaicin and Small cell Lung Cancer TherapyR15CA161491 · NCI · MARSHALL UNIVERSITY · PI DASGUPTA, PIYALI · 2012 to 2021
$1.3M
NCI NIH HHS R15 CA161491
6 · The paper itself

Abstract

The neurotransmitter acetylcholine (ACh) acts as an autocrine growth factor for human lung cancer. Several lines of evidence show that lung cancer cells express all of the proteins required for the uptake of choline (choline transporter 1, choline transporter-like proteins) synthesis of ACh (choline acetyltransferase, carnitine acetyltransferase), transport of ACh (vesicular acetylcholine transport, OCTs, OCTNs) and degradation of ACh (acetylcholinesterase, butyrylcholinesterase). The released ACh binds back to nicotinic (nAChRs) and muscarinic receptors on lung cancer cells to accelerate their proliferation, migration and invasion. Out of all components of the cholinergic pathway, the nAChR-signaling has been studied the most intensely. The reason for this trend is due to genome-wide data studies showing that nicotinic receptor subtypes are involved in lung cancer risk, the relationship between cigarette smoke and lung cancer risk as well as the rising popularity of electronic cigarettes considered by many as a "safe" alternative to smoking. There are a small number of articles which review the contribution of the other cholinergic proteins in the pathophysiology of lung cancer. The primary objective of this review article is to discuss the function of the acetylcholine-signaling proteins in the progression of lung cancer. The investigation of the role of cholinergic network in lung cancer will pave the way to novel molecular targets and drugs in this lethal malignancy.

Indexed as

AcetylcholineAdaptor Proteins, Signal TransducingAnimalsAntigens, LyCholinesterasesDisease ProgressionHumansLung NeoplasmsMembrane Transport ProteinsReceptors, MuscarinicReceptors, NicotinicSignal TransductionUrokinase-Type Plasminogen ActivatorAcetylcholineAdaptor Proteins, Signal TransducingAntigens, LyCholinesterasescholine transporterLYNX1 protein, humanMembrane Transport ProteinsReceptors, MuscarinicReceptors, NicotinicSLURP1 protein, humanUrokinase-Type Plasminogen ActivatorAcetylcholineAnti-cancer drugsCholinergicInvasionLung cancerProliferation

Identifiers

PMID30291908
PMCPMC6348061
OpenAlexW2894660607

What OpenQuestion holds

Textmetadata
LicenceTDM
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.