ArticleJournal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer2014
Overexpression of muscarinic receptor 3 promotes metastasis and predicts poor prognosis in non-small-cell lung cancer.
Article in Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 56 citations in OpenAlex.
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- Acetylcholine, Another Factor in Breast Cancer.Biology · 2023Article
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- Muscarinic Acetylcholine Receptor M3 Expression and Survival in Human Colorectal Carcinoma-An Unexpected Correlation to Guide Future Treatment?International journal of molecular sciences · 2023Article
- Mechanisms Contributing to the Comorbidity of COPD and Lung Cancer.International journal of molecular sciences · 2023Review
- The Role of the Acetylcholine System in Common Respiratory Diseases and COVID-19.Molecules (Basel, Switzerland) · 2023Review
- Blocking Muscarinic Receptor 3 Attenuates Tumor Growth and Decreases Immunosuppressive and Cholinergic Markers in an Orthotopic Mouse Model of Colorectal Cancer.International journal of molecular sciences · 2022Article
- The M3 Muscarinic Acetylcholine Receptor Promotes Epidermal Differentiation.The Journal of investigative dermatology · 2022Article
- Review
- Muscarinic Receptors Associated with Cancer.Cancers · 2022Review
- The connection between innervation and metabolic rearrangements in pancreatic cancer through serine.Frontiers in oncology · 2022Review
- Breast cancer: Muscarinic receptors as new targets for tumor therapy.World journal of clinical oncology · 2021Review
- Role of the nervous system in cancers: a review.Cell death discovery · 2021Review
- Extrasynaptic acetylcholine signaling through a muscarinic receptor regulates cell migration.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Potential Role for Combined Subtype-Selective Targeting of MFrontiers in pharmacology · 2021Review
- Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionChronic obstructive pulmonary disease (COPD) is an independent risk factor for lung cancer development, but the mechanism is not fully understood. Muscarinic receptor 3 (M3R) has been found to be involved in the progression of small-cell lung cancer and the pathological process of COPD. We hypothesized that M3R may contribute to lung cancer development, especially in patients with COPD.
methodsThe correlation between M3R expression and clinical features of non-small-cell lung cancer (NSCLC) was evaluated in 148 paraffin-embedded archived NSCLC specimens with the use of immunohistochemistry. M3R agonist and siRNA treatments were used to study the role of M3R in NSCLC cell lines. Western blotting and zymography were used to examine the impact of M3R on the PI3K/Akt/matrix metalloproteinase 9 signaling pathway.
resultsThe expression of M3R in NSCLC was significantly increased and correlated with tumor metastasis and poor survival of NSCLC patients. NSCLC patients with COPD showed higher expression of M3R than those without COPD (p = 0.0014). Moreover, M3R expression was inversely related to percent forced expiratory volume in 1 second (r = 0.7017, p < 0.0001) and forced expiratory volume in 1 second /forced vital capacity (r = 0.5057, p < 0.0001), but positively related to smoking history. Down-regulation of M3R resulted in the inhibition of migration and invasion ability of NSCLC cell lines A549 and L78. Furthermore, M3R enhanced the expression and activity of matrix metalloproteinase 9 through PI3K/Akt, which promoted the migration and invasion of NSCLC cell lines.
conclusionOur results suggest that overexpression of M3R in NSCLC promotes the progression of NSCLC, which could contribute to lung cancer development in COPD patients. M3R could be another pharmacological target in lung cancer, especially in COPD patients.
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