ArticleFrontiers in physiology2013
Nicotinic acetylcholine receptors mediate lung cancer growth.
Article in Frontiers in physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.
- Association between two CHRNA3 variants and susceptibility of lung cancer: a meta-analysis.Scientific reports · 2016Pooled it
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- The Potential and Prospects of Marine Drugs in Intervening Nerve-Tumor Crosstalk.Marine drugs · 2026Review
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- Variations in "Functional Site" Residues and Classification of Three-Finger Neurotoxins in Snake Venoms.Toxins · 2025Review
- Retroelement co-option disrupts the cancer transcriptional programme.Genome medicine · 2025Article
- Unravelling the role of tumor microenvironment responsive nanobiomaterials in spatiotemporal controlled drug delivery for lung cancer therapy.Drug delivery and translational research · 2025Review
- Nitrosamines crisis in pharmaceuticals - Insights on toxicological implications, root causes and risk assessment: A systematic review.Journal of pharmaceutical analysis · 2024Review
- Changes in the Acetylcholinesterase Enzymatic Activity in Tumor Development and Progression.Cancers · 2023Review
- Targeting CD36 determines nicotine derivative NNK-induced lung adenocarcinoma carcinogenesis.iScience · 2023Article
- Rare Missense Variants of the Human β4 Subunit Alter Nicotinic α3β4 Receptor Plasma Membrane Localisation.Molecules (Basel, Switzerland) · 2023Article
- Marine Origin Ligands of Nicotinic Receptors: Low Molecular Compounds, Peptides and Proteins for Fundamental Research and Practical Applications.Biomolecules · 2022Review
- Expression, correlation, and prognostic significance of different nicotinic acetylcholine receptors, programed death ligand 1, and dopamine receptor D2 in lung adenocarcinoma.Frontiers in oncology · 2022Article
- Rigidity of loop 1 contributes to equipotency of globular and ribbon isomers of α-conotoxin AusIA.Scientific reports · 2021Article
- α9-Containing Nicotinic Receptors in Cancer.Frontiers in cellular neuroscience · 2021Review
- Highly stable folic acid functionalized copper-nanocluster/silica nanoparticles for selective targeting of cancer cells.RSC advances · 2020Article
- α5-nAChR contributes to epithelial-mesenchymal transition and metastasis by regulating Jab1/Csn5 signalling in lung cancer.Journal of cellular and molecular medicine · 2020Article
- Differential Expression of Nicotine Acetylcholine Receptors Associates with Human Breast Cancer and Mediates Antitumor Activity of αO-Conotoxin GeXIVA.Marine drugs · 2020Article
- Article
- Proapoptotic Index Evaluation of Two Synthetic Peptides Derived from the ConeshellMarine drugs · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ion channels modulate ion flux across cell membranes, activate signal transduction pathways, and influence cellular transport-vital biological functions that are inexorably linked to cellular processes that go awry during carcinogenesis. Indeed, deregulation of ion channel function has been implicated in cancer-related phenomena such as unrestrained cell proliferation and apoptotic evasion. As the prototype for ligand-gated ion channels, nicotinic acetylcholine receptors (nAChRs) have been extensively studied in the context of neuronal cells but accumulating evidence also indicate a role for nAChRs in carcinogenesis. Recently, variants in the nAChR genes CHRNA3, CHRNA5, and CHRNB4 have been implicated in nicotine dependence and lung cancer susceptibility. Here, we silenced the expression of these three genes to investigate their function in lung cancer. We show that these genes are necessary for the viability of small cell lung carcinomas (SCLC), the most aggressive type of lung cancer. Furthermore, we show that nicotine promotes SCLC cell viability whereas an α3β4-selective antagonist, α-conotoxin AuIB, inhibits it. Our findings posit a mechanism whereby signaling via α3/α5/β4-containing nAChRs promotes lung carcinogenesis.
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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.