ArticleCellular and molecular life sciences : CMLS2023
Acetylcholine promotes chronic stress-induced lung adenocarcinoma progression via α5-nAChR/FHIT pathway.
Article in Cellular and molecular life sciences : CMLS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 19 citations in OpenAlex.
- Targeting the nervous system: Mechanistic insights into neuro-tumor communication and therapeutic opportunities.Acta pharmaceutica Sinica. B · 2026Review
- Neural regulation in lung cancer: from mechanisms to new therapeutic perspectives.Clinical and experimental medicine · 2026Review
- Zinc finger protein-associated gene signature serves as a potential predictor for prognosis and therapeutic response in lung adenocarcinoma.Amino acids · 2026Article
- Norepinephrine promotes lung cancer cell progression via PFKFB3-promoted histone lactylation-mediated activation of the NF-κB signaling pathway.Open life sciences · 2026Article
- Neurotransmitters and Immunity: Molecular Mechanisms, Biological Functions, Diseases, and Potential Therapeutic Targets.MedComm · 2025Review
- The role of acetylcholine and its receptors in tumor immune regulation: mechanisms and potential therapeutic targets.Molecular cancer · 2025Review
- Histidine metabolism drives liver cancer progression via immune microenvironment modulation through metabolic reprogramming.Journal of translational medicine · 2025Article
- Epigenetic modifications in early stage lung cancer: pathogenesis, biomarkers, and early diagnosis.MedComm · 2025Review
- α5-nAChR/NETO2 contributed to chronic stress-promoted lung adenocarcinoma progression.Cancer cell international · 2025Article
- Decoding the metastatic nexus: how chronic stress reprograms neuroendocrine-metabolic-microbiome circuits to fuel tumor metastasis.American journal of cancer research · 2025Review
- Perspectives on the α5 nicotinic acetylcholine receptor in lung cancer progression.Frontiers in cell and developmental biology · 2025Review
- Nicotine promotes M2 macrophage polarization through α5-nAChR/SOX2/CSF-1 axis in lung adenocarcinoma.Cancer immunology, immunotherapy : CII · 2024Article
- α5-nAChR/ADAM10 signaling mediates nicotine-related cutaneous melanoma progression via STAT3 activation.Archives of dermatological research · 2024Article
- Alpha5 nicotine acetylcholine receptor subunit promotes intrahepatic cholangiocarcinoma metastasis.Signal transduction and targeted therapy · 2024Article
- Comprehensive assessment of base excision repair (BER)-related lncRNAs as prognostic and functional biomarkers in lung adenocarcinoma: implications for personalized therapeutics and immunomodulation.Journal of cancer research and clinical oncology · 2023Article
- The expression of nicotinic acetylcholine receptor subunits and their associations with local immune cells and prognosis in oral squamous cell carcinoma.Cancer medicine · 2023Article
- Investigating the crosstalk between chronic stress and immune cells: implications for enhanced cancer therapy.Frontiers in neuroscience · 2023Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Chronic stress significantly elevates the expression levels of various neurotransmitters in the tumour microenvironment, thereby promoting the cell growth and metastasis of lung adenocarcinoma (LUAD). However, the role of chronic stress in the progression of LUAD remains unclear. In this study, we found that chronic restraint stress increases the levels of the neurotransmitter acetylcholine (ACh), and the α5-nicotinic acetylcholine receptor (α5-nAChR) and decreased fragile histidine triad (FHIT) expression in vivo. Crucially, the increased ACh levels promoted LUAD cell migration and invasion via modulation of the α5-nAChR/DNA methyltransferase 1 (DNMT1)/FHIT axis. In a chronic unpredictable stress (CUMS) mouse model, chronic stress promotes tumour development, accompanied by changes in α5-nAChR, DNMT1, FHIT, and vimentin. Together, these findings reveal a novel chronic stress-mediated LUAD signalling pathway: chronic stress enforces lung adenocarcinoma cell invasion and migration via the ACh/α5-nAChR/FHIT axis, which could be a potential therapeutic target for chronic stress-related LUAD.
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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.