ArticleAmerican journal of physiology. Cell physiology2017
Aspirin therapy reduces the ability of platelets to promote colon and pancreatic cancer cell proliferation: Implications for the oncoprotein c-MYC.
Article in American journal of physiology. Cell physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
53 citing papers in PubMed, 2 syntheses or guidelines pooled it, 84 citations in OpenAlex.
- Aspirin Use and Common Cancer Risk: A Meta-Analysis of Cohort Studies and Randomized Controlled Trials.Frontiers in oncology · 2021Pooled it
- Aspirin use and pancreatic cancer risk: A systematic review of observational studies.Medicine · 2019Pooled it
- Platelets as regulators of anti-tumor immunity: mechanisms and clinical implications.Cancer metastasis reviews · 2026Review
- Investigating the effects of platelets, platelet releasate and aspirin on colorectal cancer cell proliferation, migration and invasion.Medical oncology (Northwood, London, England) · 2026Article
- The inhibitory action of camel urine on human platelet surface glycoproteins could be the potential mechanism for its reported anticancer effects.Frontiers in pharmacology · 2026Article
- Genomic and cellular responses to aspirin in colonic organoids from African- and European-Americans.Physiological genomics · 2025Article
- Article
- The role of platelets in cancer: from their influence on tumor progression to their potential use in liquid biopsy.Biomarker research · 2025Review
- Aspirin in Cancer Therapy: Pharmacology and Nanotechnology Advances.International journal of nanomedicine · 2025Review
- O-GlcNAcylation: Crosstalk between Hemostasis, Inflammation, and Cancer.International journal of molecular sciences · 2024Review
- Platelet-lymphocyte ratio predicts chemotherapy response and prognosis in patients with gastric cancer undergoing radical resection.Frontiers in oncology · 2024Article
- Theoretical basis validation and oxidative stress markers for cancer prevention clinical trials of aspirin.Scientific reports · 2023Article
- Genomic and epigenomic responses to aspirin in human colonic organoids.Physiological genomics · 2023Article
- Article
- Colorectal cancer chemoprevention: is aspirin still in the game?Cancer biology & therapy · 2022Review
- Inter-agency perspective: Translating advances in biomarker discovery and medical countermeasures development between terrestrial and space radiation environments.Life sciences in space research · 2022Article
- Pancreatic Cancer Cells Induce MicroRNA Deregulation in Platelets.International journal of molecular sciences · 2022Article
- Challenges and Opportunities Associated With Platelets in Pancreatic Cancer.Frontiers in oncology · 2022Review
- Unlabeled aspirin as an activatable theranostic MRI agent for breast cancer.Theranostics · 2022Article
- Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Aspirin, an anti-inflammatory and antithrombotic drug, has become the focus of intense research as a potential anticancer agent owing to its ability to reduce tumor proliferation in vitro and to prevent tumorigenesis in patients. Studies have found an anticancer effect of aspirin when used in low, antiplatelet doses. However, the mechanisms through which low-dose aspirin works are poorly understood. In this study, we aimed to determine the effect of aspirin on the cross talk between platelets and cancer cells. For our study, we used two colon cancer cell lines isolated from the same donor but characterized by different metastatic potential, SW480 (nonmetastatic) and SW620 (metastatic) cancer cells, and a pancreatic cancer cell line, PANC-1 (nonmetastatic). We found that SW480 and PANC-1 cancer cell proliferation was potentiated by human platelets in a manner dependent on the upregulation and activation of the oncoprotein c-MYC. The ability of platelets to upregulate c-MYC and cancer cell proliferation was reversed by an antiplatelet concentration of aspirin. In conclusion, we show for the first time that inhibition of platelets by aspirin can affect their ability to induce cancer cell proliferation through the modulation of the c-MYC oncoprotein.
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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.