ReviewInternational journal of molecular sciences2021
Differential Actions of Muscarinic Receptor Subtypes in Gastric, Pancreatic, and Colon Cancer.
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 35 citations in OpenAlex.
- Anisodus tanguticus in Cancer Research: A Review of Traditional Use, Phytochemistry, Extraction Methods, and Preclinical Antitumor Evidence.Medical science monitor : international medical journal of experimental and clinical research · 2026Review
- Antispasmodic Activity of Green-Synthesized Phenylaminojuglones: In Vitro and In Silico Studies.ACS omega · 2026Article
- Selective modulation of murine intestinal MAmerican journal of physiology. Cell physiology · 2026Article
- Bile acid signaling: from dynamic pool composition to inter-organ communication.Frontiers in endocrinology · 2026Review
- Transcriptomic insights into loperamide-induced gastric dysmotility: RNA-seq analysis of a mouse model.Frontiers in physiology · 2026Article
- Nervous Breakdown: Chronic Inflammatory Demyelinating Polyneuropathy as an Extra-Intestinal Manifestation of Ulcerative Colitis.Digestive diseases and sciences · 2025Article
- Neurotransmitter Regulatory Networks: A New Perspective on Cancer Therapy.Biomolecules · 2025Review
- The role of acetylcholine and its receptors in tumor immune regulation: mechanisms and potential therapeutic targets.Molecular cancer · 2025Review
- The Role of Xenobiotics and Anelloviruses in Colorectal Cancer: Mechanisms and Perspectives.International journal of molecular sciences · 2025Review
- Targeting Bile-Acid Metabolism: Nutritional and Microbial Approaches to Alleviate Ulcerative Colitis.Nutrients · 2025Review
- A New Era of Muscarinic Acetylcholine Receptor Modulators in Neurological Diseases, Cancer and Drug Abuse.Pharmaceuticals (Basel, Switzerland) · 2025Review
- AMPs inhibit the proliferation, migration, and invasion of lung cancer via the CHRM3/PI3K/AKT and CHRM3/MAPK pathways.Frontiers in oncology · 2025Article
- Role and value of the tumor microenvironment in the progression and treatment resistance of gastric cancer (Review).Oncology reports · 2025Review
- Darifenacin: a promising chitinase 3-like 1 inhibitor to tackle drug resistance in pancreatic ductal adenocarcinoma.Cancer chemotherapy and pharmacology · 2024Article
- Cholinergic Mechanisms in Gastrointestinal Neoplasia.International journal of molecular sciences · 2024Review
- Bile acid metabolism and signaling in health and disease: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Targeting Farnesoid X Receptor in Tumor and the Tumor Microenvironment: Implication for Therapy.International journal of molecular sciences · 2023Review
- Biglycan regulated colorectal cancer progress by modulating enteric neuron-derived IL-10 and abundance ofiScience · 2023Article
- Saikosaponin D reverses epinephrine- and norepinephrine-induced gemcitabine resistance in intrahepatic cholangiocarcinoma by downregulating ADRB2/glycolysis signaling.Acta biochimica et biophysica Sinica · 2023Article
- The effect of butylscopolamine on [EJNMMI research · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Cancers arising from gastrointestinal epithelial cells are common, aggressive, and difficult to treat. Progress in this area resulted from recognizing that the biological behavior of these cancers is highly dependent on bioactive molecules released by neurocrine, paracrine, and autocrine mechanisms within the tumor microenvironment. For many decades after its discovery as a neurotransmitter, acetylcholine was thought to be synthesized and released uniquely from neurons and considered the sole physiological ligand for muscarinic receptor subtypes, which were believed to have similar or redundant actions. In the intervening years, we learned this former dogma is not tenable. (1) Acetylcholine is not produced and released only by neurons. The cellular machinery required to synthesize and release acetylcholine is present in immune, cancer, and other cells, as well as in lower organisms (e.g., bacteria) that inhabit the gut. (2) Acetylcholine is not the sole physiological activator of muscarinic receptors. For example, selected bile acids can modulate muscarinic receptor function. (3) Muscarinic receptor subtypes anticipated to have overlapping functions based on similar G protein coupling and downstream signaling may have unexpectedly diverse actions. Here, we review the relevant research findings supporting these conclusions and discuss how the complexity of muscarinic receptor biology impacts health and disease, focusing on their role in the initiation and progression of gastric, pancreatic, and colon cancers.
Indexed as
Identifiers
What OpenQuestion holds
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.