Evidence map›Paper›PMID 28726253›Full record

ArticleBritish journal of pharmacology2018

α9- and α7-containing receptors mediate the pro-proliferative effects of nicotine in the A549 adenocarcinoma cell line.

Vanessa Mucchietto, Francesca Fasoli, Susanna Pucci, Milena Moretti, Roberta Benfante, Annalisa Maroli, Simona Di Lascio, Cristiano Bolchi, Marco Pallavicini, Cheryl Dowell and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 7% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

  1. Pooled it
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  17. Article
  18. Effect of Nicotine on Immune System Function.Advanced pharmaceutical bulletin · 2023
    Review
  19. Marine drugs · 2022
    Review
  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

13 authors at 3 institutions in 2 countries.

Vanessa MucchiettoCNR, Institute of Neuroscience, Milan, Italy.
Francesca FasoliCNR, Institute of Neuroscience, Milan, Italy.
Susanna PucciCNR, Institute of Neuroscience, Milan, Italy.
Milena MorettiCNR, Institute of Neuroscience, Milan, Italy.
Roberta BenfanteCNR, Institute of Neuroscience, Milan, Italy.
Annalisa MaroliDepartment of Medical Biotechnology and Translational Medicine, Università degli Studi di Milano, Milan, Italy.
Simona Di LascioDepartment of Medical Biotechnology and Translational Medicine, Università degli Studi di Milano, Milan, Italy.
Cristiano BolchiDepartment of Pharmaceutical Science, Università degli Studi di Milano, Milan, Italy.
Marco PallaviciniDepartment of Pharmaceutical Science, Università degli Studi di Milano, Milan, Italy.
Cheryl DowellDepartment of Biology, University of Utah, Salt Lake City, UT, USA.
Michael McIntoshDepartment of Biology, University of Utah, Salt Lake City, UT, USA.
Francesco ClementiCNR, Institute of Neuroscience, Milan, Italy.
Cecilia GottiCNR, Institute of Neuroscience, Milan, Italy.ORCID 0000-0001-5358-8643
University of Milan · ITNeuroscience Institute · ITUniversity of Utah · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeTobacco smoke contains many classes of carcinogens and although nicotine is unable to initiate tumourigenesis in humans and rodents, it promotes tumour growth and metastasis in lung tumours by acting on neuronal nicotinic ACh receptors (nAChRs). The aim of this study was to identify molecularly, biochemically and pharmacologically which nAChR subtypes are expressed and functionally activated by nicotine in lung cancer cell lines. EXPERIMENTAL APPROACH: We used A549 and H1975 adenocarcinoma cell lines derived from lung tumours to test the in vitro effects of nicotine, and nAChR subtype-specific peptides and compounds. KEY

resultsThe two adenocarcinoma cell lines express distinctive nAChR subtypes, and this affects their nicotine-induced proliferation. In A549 cells, nAChRs containing the α7 or α9 subunits not only regulate nicotine-induced cell proliferation but also the activation of the Akt and ERK pathways. Blocking these nAChRs by means of subtype-specific peptides, or silencing their expression by means of subunit-specific siRNAs, abolishes nicotine-induced proliferation and signalling. Moreover, we found that the α7 antagonist MG624 also acts on α9-α10 nAChRs, blocks the effects of nicotine on A549 cells and has dose-dependent cytotoxic activity. CONCLUSIONS AND IMPLICATIONS: These results highlight the pathophysiological role of α7- and α9-containing receptors in promoting non-small cell lung carcinoma cell growth and intracellular signalling and provide a framework for the development of new drugs that specifically target the receptors expressed in lung tumours. LINKED ARTICLES: This article is part of a themed section on Nicotinic Acetylcholine Receptors. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.11/issuetoc.

Indexed as

A549 CellsAdenocarcinomaalpha7 Nicotinic Acetylcholine ReceptorCell Line, TumorCell ProliferationDose-Response Relationship, DrugHumansLung NeoplasmsNicotineQuaternary Ammonium CompoundsReceptors, NicotinicStilbenesStructure-Activity Relationshipalpha7 Nicotinic Acetylcholine ReceptorChrna7 protein, humanCHRNA9 protein, humanNicotineQuaternary Ammonium CompoundsReceptors, NicotinicStilbenestriethyl-(beta-4-stilbenoxyethyl)ammonium

Identifiers

PMID28726253
PMCPMC5980168
OpenAlexW2739176213

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.