ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016
Muscarinic receptor M3 mediates cell proliferation induced by acetylcholine and contributes to apoptosis in gastric cancer.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 52 citations in OpenAlex.
- The Serotonergic and Cholinergic Signaling Pathways Drive Gastric Precancerous Lesions and Its Potential Mechanism.Cancer science · 2026Article
- Gastric Cancer: Pathobiology and Therapeutics.MedComm · 2026Review
- Peripheral nerve remodeling in the tumor microenvironment: neuro-immune crosstalk, molecular mechanisms, and precision therapeutic.Frontiers in immunology · 2026Review
- Influence of the Cholinergic System on the Pathogenesis of Glioblastoma: Impact of the Neutrophil Granulocytes.International journal of molecular sciences · 2025Article
- Neurotransmitters and Immunity: Molecular Mechanisms, Biological Functions, Diseases, and Potential Therapeutic Targets.MedComm · 2025Review
- Advances in the study of the relationship between neurotransmitters and gastric cancer.World journal of gastroenterology · 2025Review
- Mapping the global research landscape of perineural invasion in gastrointestinal malignancies: a bibliometric visualization analysis.Discover oncology · 2025Article
- Aberrant PJA2-CHRM3 signaling creates a therapeutic vulnerability in gastric tumor.British journal of cancer · 2025Article
- Comparative Analysis of Cholinergic Machinery in Carcinomas: Discovery of Membrane-Tethered ChAT as Evidence for Surface-Based ACh Synthesis in Neuroblastoma Cells.International journal of molecular sciences · 2025Article
- Neurotransmitter Regulatory Networks: A New Perspective on Cancer Therapy.Biomolecules · 2025Review
- Metabolomic changes associated with treatment response of neoadjuvant chemotherapy with TEC regimen in HER2-negative breast cancer.Frontiers in pharmacology · 2025Article
- Cholinergic Mechanisms in Gastrointestinal Neoplasia.International journal of molecular sciences · 2024Review
- Understanding the role of nerves in head and neck cancers - a review.Oncology reviews · 2024Review
- Changes in the Acetylcholinesterase Enzymatic Activity in Tumor Development and Progression.Cancers · 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
- Nerves in gastrointestinal cancer: from mechanism to modulations.Nature reviews. Gastroenterology & hepatology · 2022Review
- Review
- Review
- Differential Actions of Muscarinic Receptor Subtypes in Gastric, Pancreatic, and Colon Cancer.International journal of molecular sciences · 2021Review
- Exploiting unique features of the gut-brain interface to combat gastrointestinal cancer.The Journal of clinical investigation · 2021Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The muscarinic receptor M3 is an acetylcholine receptor that regulates the activity of numerous fundamental central and peripheral nervous system functions. Recent studies have identified the activation of the M3 receptor in several cancers; however, the role of M3 in human gastric cancer (GC) remains largely unknown. In this study, we demonstrated that the M3 receptor was overexpressed in human GC tissues and was correlated with the cancer stage and with lymph node metastasis. In vitro, the M3 receptor enhanced the proliferation induced by acetylcholine in human GC cells, whereas the knockdown of M3 by a small hairpin RNA (shRNA) inhibited cell proliferation. Furthermore, M3 knockdown caused G2/M phase cell cycle arrest and induced apoptosis in human GC cells. In vivo, M3 knockdown suppressed tumorigenesis and promoted apoptosis in GC xenografts. In addition, we also detected the secretion of acetylcholine (ACh) by human GC cells and observed the co-expression of the M3 receptor and choline acetyltransferase (ChAT), the enzyme necessary for acetylcholine synthesis, in human GC tissues and cells. Taken together, our findings support an oncogenic role for the M3 receptor in gastric cancer, suggesting that M3 antagonists may serve as potential adjuvants to GC therapies. Further study of the underlying molecular mechanism could also lead to the identification of novel therapeutic targets for improved treatment of GC.
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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.