ArticleCell proliferation2008
Role of alpha7-nicotinic acetylcholine receptor in human non-small cell lung cancer proliferation.
Article in Cell proliferation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 41 papers.
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.
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.
Who cites it
41 citing papers in PubMed, 83 citations in OpenAlex.
- Downregulation of Stem-Loop Binding Protein by Nicotine via α7-Nicotinic Acetylcholine Receptor and Its Role in Nicotine-Induced Cell Transformation.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- Inflammation Regulation via an Agonist and Antagonists of α7 Nicotinic Acetylcholine Receptors in RAW264.7 Macrophages.Marine drugs · 2022Article
- Eyelid carcinomas: Tumor aggressiveness tendencies for smokers compared to non-smokers.Experimental and therapeutic medicine · 2022Article
- Nicotinic-nAChR signaling mediates drug resistance in lung cancer.Journal of Cancer · 2020Review
- What are the respiratory effects of e-cigarettes?BMJ (Clinical research ed.) · 2019Review
- miR-499 released during myocardial infarction causes endothelial injury by targeting α7-nAchR.Journal of cellular and molecular medicine · 2019Article
- Genome-wide association analysis for β-hydroxybutyrate concentration in Milk in Holstein dairy cattle.BMC genetics · 2019Article
- Chronic nicotine exposure affects programmed death-ligand 1 expression and sensitivity to epidermal growth factor receptor-tyrosine kinase inhibitor in lung cancer.Translational cancer research · 2019Article
- The effects of cigarette smoking extracts on cell cycle and tumor spread: novel evidence.Future science OA · 2019Review
- Mining and validating the expression pattern and prognostic value of acetylcholine receptors in non-small cell lung cancer.Medicine · 2019Observational
- α-Conotoxin ImI-modified polymeric micelles as potential nanocarriers for targeted docetaxel delivery to α7-nAChR overexpressed non-small cell lung cancer.Drug delivery · 2018Article
- APS8 Delays Tumor Growth in Mice by Inducing Apoptosis of Lung Adenocarcinoma Cells Expressing High Number of α7 Nicotinic Receptors.Marine drugs · 2018Article
- α7 nicotinic acetylcholine receptors in lung cancer.Oncology letters · 2018Review
- Expression patterns for nicotinic acetylcholine receptor subunit genes in smoking-related lung cancers.Oncotarget · 2017Article
- The Role of Nitrosamine (NNK) in Breast Cancer Carcinogenesis.Journal of mammary gland biology and neoplasia · 2017Review
- Chronic electronic cigarette exposure in mice induces features of COPD in a nicotine-dependent manner.Thorax · 2016Article
- β-Cryptoxanthin Reduced Lung Tumor Multiplicity and Inhibited Lung Cancer Cell Motility by Downregulating Nicotinic Acetylcholine Receptor α7 Signaling.Cancer prevention research (Philadelphia, Pa.) · 2016Article
- Comprehensive review of epidemiological and animal studies on the potential carcinogenic effects of nicotine per se.Critical reviews in toxicology · 2016Review
- Nicotinic acetylcholine receptors and cancer.Biomedical reports · 2016Article
- Will chronic e-cigarette use cause lung disease?American journal of physiology. Lung cellular and molecular physiology · 2015Review
Corrections and comments
- Retraction · 2017-08-29Falsification/Fabrication of Data · Investigation by Company/Institution ·
- Erratum issued
- Erratum issued
- Retracted
Authors and funding
12 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesLung cancer is the most common cause of cancer death in the world. Cigarette smoking represents the major risk factor. Nicotine, an active component of cigarettes, can induce cell proliferation, angiogenesis and apoptosis resistance. All these events are mediated through the nicotinic acetylcholine receptor (nAChR) expressed on lung cancer cells. We speculate that new insights into the pathophysiological roles of nAChR may lead to new therapeutic avenues to reduce non-small cell lung cancer (NSCLC) tumour growth. MATERIALS AND
methodsHuman samples of NSCLC, cell lines and mouse models were utilized in Western blotting, reverse transcriptase polymerase chain reaction and apoptosis studies.
resultsHuman NSCLC tissues expressed alpha7-nAChR. This expression was higher in smoking patients with squamous carcinomas than those with adenocarcinomas and in male smoking patients than in females. All the data support the hypothesis that major expression of alpha7-nAChR is related to major activation of the Rb-Raf-1/phospho-ERK/phospho-p90RSK pathway. alpha7-nAChR antagonists, via mitochondria associated apoptosis, inhibited proliferation of human NSCLC primary and established cells. Nicotine stimulates tumour growth in a murine model, A549 cells orthotopically grafted. The effects of nicotine were associated with increases in phospho-ERK in tumours. Proliferation effects of nicotine could be blocked by inhibition of alpha7-nAChR by the high affinity ligand alpha-cobratoxin.
conclusionThese results showed that alpha7-nAChR plays an important role in NSCLC cell growth and tumour progression as well as in cell death.
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Registered trials
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.