Evidence map›Paper›PMID 36361620›Full record

ArticleInternational journal of molecular sciences2022

Regulation of Cisplatin Resistance in Lung Cancer Cells by Nicotine, BDNF, and a β-Adrenergic Receptor Blocker.

Ravel Ray, Hind Al Khashali, Ben Haddad, Jadziah Wareham, Kai-Ling Coleman, Danyah Alomari, Robert Ranzenberger, Jeffrey Guthrie, Deborah Heyl, Hedeel Guy Evans

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.0field-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

25 citing papers in PubMed, 35 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

10 authors at 1 institution in 1 country.

Ravel RayChemistry Department, Eastern Michigan University, Ypsilanti, MI 48197, USA.
Hind Al KhashaliChemistry Department, Eastern Michigan University, Ypsilanti, MI 48197, USA.
Ben HaddadChemistry Department, Eastern Michigan University, Ypsilanti, MI 48197, USA.
Jadziah WarehamChemistry Department, Eastern Michigan University, Ypsilanti, MI 48197, USA.
Kai-Ling ColemanChemistry Department, Eastern Michigan University, Ypsilanti, MI 48197, USA.
Danyah AlomariChemistry Department, Eastern Michigan University, Ypsilanti, MI 48197, USA.
Robert RanzenbergerChemistry Department, Eastern Michigan University, Ypsilanti, MI 48197, USA.
Jeffrey GuthrieChemistry Department, Eastern Michigan University, Ypsilanti, MI 48197, USA.
Deborah HeylChemistry Department, Eastern Michigan University, Ypsilanti, MI 48197, USA.
Hedeel Guy EvansChemistry Department, Eastern Michigan University, Ypsilanti, MI 48197, USA.ORCID 0000-0002-7970-9084
Eastern Michigan University · US

Funding

Probing the Role of Insulin-Like Growth Factor-Binding Protein 3 and Humanin in Regulating Hyaluronan FunctionR15GM131222 · NIGMS · EASTERN MICHIGAN UNIVERSITY · PI GUY EVANS, HEDEEL I. · 2019 to 2025
$1.5M
NIGMS NIH HHS R15 GM131222NIH HHS R15GM131222
6 · The paper itself

Abstract

It is well-recognized that cigarette smoking is a primary risk factor in the development of non-small cell lung cancer (NSCLC), known to account for ~80% of all lung cancers with nicotine recognized as the major addictive component. In investigating the effect of nicotine, brain-derived neurotrophic factor (BDNF), and the β-adrenergic receptor blocker, propranolol, on sensitivity of NSCLC cell lines, A549 and H1299, to cisplatin, we found increased cell viability, and enhanced cisplatin resistance with nicotine and/or BDNF treatment while opposite effects were found upon treatment with propranolol. Cell treatment with epinephrine or nicotine led to EGFR and IGF-1R activation, effects opposite to those found with propranolol. Blocking EGFR and IGF-1R activation increased cell sensitivity to cisplatin in both cell lines. PI3K and AKT activities were upregulated by nicotine or BDNF and downregulated by cell treatment with inhibitors against EGFR and IGF-1R and by propranolol. Apoptosis and cell sensitivity to cisplatin increased upon co-treatment of cells with cisplatin and inhibitors against PI3K or AKT. Our findings shed light on an interplay between nicotine, BDNF, and β-Adrenergic receptor signaling in regulating survival of lung cancer cells and chemoresistance which can likely expand therapeutic opportunities that target this regulatory network in the future.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsAdrenergic AntagonistsBrain-Derived Neurotrophic FactorCell Line, TumorCisplatinDrug Resistance, NeoplasmErbB ReceptorsHumansNicotinePhosphatidylinositol 3-KinasesPropranololProto-Oncogene Proteins c-aktReceptors, Adrenergic, betaAdrenergic AntagonistsBrain-Derived Neurotrophic FactorCisplatinErbB ReceptorsNicotinePhosphatidylinositol 3-KinasesPropranololProto-Oncogene Proteins c-aktReceptors, Adrenergic, betabrain-derived neurotrophic factorchemoresistancecisplatinEGFRIGF-1Rlung cancernicotinePI3K/AKTβ-adrenergic receptors

Identifiers

PMID36361620
PMCPMC9657603
OpenAlexW4307262627

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.