ArticleBMC cancer2015
Aspirin and P2Y12 inhibition attenuate platelet-induced ovarian cancer cell invasion.
Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 2 of them syntheses that pooled it.
What it found
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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
40 citing papers in PubMed, 2 syntheses or guidelines pooled it, 72 citations in OpenAlex.
- The Anti-Metastatic Role of Aspirin in Cancer: A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Aspirin Use and Mortality in Women With Ovarian Cancer: A Meta-Analysis.Frontiers in oncology · 2020Pooled it
- Trial
- Platelet extravasation in the microvasculature: an under-appreciated role for platelets.Frontiers in immunology · 2026Review
- Tumor-associated macrophages and platelets in tumor microenvironment and its potential therapeutic role in ovarian cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Modelling the ageing dependence of cancer evolutionary trajectories.Nature reviews. Cancer · 2025Review
- Role and recent progress of P2Y12 receptor in cancer development.Purinergic signalling · 2025Review
- 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
- Circulating tumor cells: from new biological insights to clinical practice.Signal transduction and targeted therapy · 2024Review
- Platelet and epithelial cell interations can be modeled in cell culture, and are not affected by dihomo-gamma-linolenic acid.PloS one · 2024Article
- Liquid biopsies for cancer: From bench to clinic.MedComm · 2023Review
- Review
- Article
- Review
- Emerging roles of platelets in cancer biology and their potential as therapeutic targets.Frontiers in oncology · 2022Review
- Aspirin Suppressed PD-L1 Expression through Suppressing KAT5 and Subsequently Inhibited PD-1 and PD-L1 Signaling to Attenuate OC Development.Journal of oncology · 2022Article
- Human tumor microenvironment chip evaluates the consequences of platelet extravasation and combinatorial antitumor-antiplatelet therapy in ovarian cancer.Science advances · 2021Article
- Inflammatory cell-associated tumors. Not only macrophages (TAMs), fibroblasts (TAFs) and neutrophils (TANs) can infiltrate the tumor microenvironment. The unique role of tumor associated platelets (TAPs).Cancer immunology, immunotherapy : CII · 2021Review
- P2Y receptors for extracellular nucleotides: Contributions to cancer progression and therapeutic implications.Biochemical pharmacology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPlatelet-cancer cell interactions play a key role in successful haematogenous metastasis. Disseminated malignancy is the leading cause of death among ovarian cancer patients. It is unknown why different ovarian cancers have different metastatic phenotypes. To investigate if platelet-cancer cell interactions play a role, we characterized the response of ovarian cancer cell lines to platelets both functionally and at a molecular level.
methodsCell lines 59 M and SK-OV-3 were used as in vitro model systems of metastatic ovarian cancer. Platelet cloaking of each cell line was quantified by flow cytometry. Matrigel invasion chamber assays were used to assess the invasive capacity of the cell lines. The induction of an EMT was assessed by morphology analysis and by gene expression analysis of a panel of 11 EMT markers using TaqMan RT-PCR.
resultsSK-OV-3 cells adhered to and activated more platelets than 59 M cells (p = 0.0333). Platelets significantly promoted the ability of only SK-OV-3 cells to invade (p ≤ 0.0001). Morphology and transcritpome analysis indicated that platelets induce an epithelial-to-mesenchymal transition phenotype in both cells lines, with a more exaggerated response in SK-OV-3 cells. Next, we investigated if antiplatelet agents could abrogate the platelet-induced aggressive phenotype in SK-OV-3 cells. Both aspirin (p ≤ 0.05) and 2-methylthioadenosine 5'-monophosphate triethylammonium salt hydrate (P2Y12 inhibitor; p ≤ 0.01) significantly decreased their invasion capacity, and effectively reverted invasion to levels comparable to SK-OV-3 cells alone.
conclusionWhile there is increasing evidence for the cancer-protective effect of aspirin, this study suggests P2Y12 inhibition may also play a role. Understanding these complex interactions between platelets and cancer cells could ultimately allow the establishment of therapies tailored to inhibiting metastasis, thus significantly reducing cancer morbidity.
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