ArticlePurinergic signalling2016
Adenosine arrests breast cancer cell motility by A3 receptor stimulation.
Article in Purinergic signalling, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Role of ENPP1 in cancer pathogenesis: Mechanisms and clinical implications (Review).Oncology letters · 2024Review
- Genetic and functional modulation by agonist MRS5698 and allosteric enhancer LUF6000 at the native APurinergic signalling · 2024Article
- Adenosine receptors in breast cancer.Molecular biology reports · 2024Review
- Species dependence of APurinergic signalling · 2023Review
- From Myricetin to the Discovery of Novel Natural Human ENPP1 Inhibitors: A Virtual Screening, Molecular Docking, Molecular Dynamics Simulation, and MM/GBSA Study.Molecules (Basel, Switzerland) · 2022Article
- Drugs Targeting the A3 Adenosine Receptor: Human Clinical Study Data.Molecules (Basel, Switzerland) · 2022Review
- Autocrine and paracrine purinergic signaling in the most lethal types of cancer.Purinergic signalling · 2021Review
- From purines to purinergic signalling: molecular functions and human diseases.Signal transduction and targeted therapy · 2021Review
- Morphological and Motility Features of the Stable Bleb-Driven Monopodial Form ofInfection and immunity · 2020Article
- Purinergic Signaling in the Hallmarks of Cancer.Cells · 2020Review
- Inhibition of the Adenosinergic Pathway in Cancer Rejuvenates Innate and Adaptive Immunity.International journal of molecular sciences · 2019Review
- Targeting Adenosine in Cancer Immunotherapy to Enhance T-Cell Function.Frontiers in immunology · 2019Review
- AMedicinal research reviews · 2018Review
- Pathological overproduction: the bad side of adenosine.British journal of pharmacology · 2017Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
In neutrophils, adenosine triphosphate (ATP) release and autocrine purinergic signaling regulate coordinated cell motility during chemotaxis. Here, we studied whether similar mechanisms regulate the motility of breast cancer cells. While neutrophils and benign human mammary epithelial cells (HMEC) form a single leading edge, MDA-MB-231 breast cancer cells possess multiple leading edges enriched with A3 adenosine receptors. Compared to HMEC, MDA-MB-231 cells overexpress the ectonucleotidases ENPP1 and CD73, which convert extracellular ATP released by the cells to adenosine that stimulates A3 receptors and promotes cell migration with frequent directional changes. However, exogenous adenosine added to breast cancer cells or the A3 receptor agonist IB-MECA dose-dependently arrested cell motility by simultaneous stimulation of multiple leading edges, doubling cell surface areas and significantly reducing migration velocity by up to 75 %. We conclude that MDA-MB-231 cells, HMEC, and neutrophils differ in the purinergic signaling mechanisms that regulate their motility patterns and that the subcellular distribution of A3 adenosine receptors in MDA-MB-231 breast cancer cells contributes to dysfunctional cell motility. These findings imply that purinergic signaling mechanisms may be potential therapeutic targets to interfere with the motility of breast cancer cells in order to reduce the spread of cancer cells and the risk of metastasis.
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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.