ArticleCell communication and signaling : CCS2024
Platelet-derived extracellular vesicles induced through different activation pathways drive melanoma progression by functional and transcriptional changes.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The research landscape and evolutionary trends of platelet-derived extracellular vesicles: a bibliometric and LDA analysis (2015-2026).Frontiers in oncology · 2026Pooled it
- Artificial intelligence and extracellular vesicles in oncology: towards tumor diagnosis, prediction, and therapy.Drug delivery · 2026Review
- Tumor-platelet cross talk in cancer: mechanisms, thrombotic risk, and translational opportunities.Blood advances · 2026Review
- Platelet-neutrophil cooperation in cancer: mechanisms of metastatic niche formation and implications for prognostic stratification and therapy.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- Research advances on platelet glycoprotein VI in ischemic stroke.Thrombosis journal · 2026Review
- Microvesicles, exosomes and their combinations with cytoplasmic organelles: from their discovery to their innovative roles in clinical medicine.Biology direct · 2026Review
- The Duality of Collagens in Metastases of Solid Tumors.International journal of molecular sciences · 2025Review
- Review
- Correction: Platelet-derived extracellular vesicles induced through different activation pathways drive melanoma progression by functional and transcriptional changes.Cell communication and signaling : CCS · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBeyond their conventional roles in hemostasis and wound healing, platelets have been shown to facilitate hematogenous metastasis by interacting with cancer cells. Depending on the activation route, platelets also generate different platelet-derived extracellular vesicles (PEVs) that may educate cancer cells in the circulation or within the tumor microenvironment. We engaged different platelet-activating receptors, including glycoprotein VI and C-type lectin-like receptor 2, to generate a spectrum of PEV types. This allowed us to investigate the differential capacity of PEVs to alter cancer hallmark functions such as proliferation, invasion, and pro-angiogenic potential using melanoma as a model. Additionally, we analyzed changes in the cell transcriptomes and cancer EV profiles.
methodsTwo human melanoma cell lines (MV3 and A2058) with differential metastatic potential were studied in the 3D spheroid cultures. Human platelets were activated with collagen related peptide (CRP), fucoidan from Fucus vesiculosus (FFV), thrombin & collagen co-stimulus and Ca
resultsAmong the studied PEVs, those generated by CRP and FFV exhibited the most pronounced effects on altering cancer hallmark functions. Specifically, CRP and FFV PEVs increased proliferation in both MV3 and A2058 spheroids. Distinct tetraspanin signatures of melanoma EVs were induced by all PEV types. While the PI3K-Akt and MAPK signaling pathways were activated by both CRP and FFV PEVs, they differently upregulated the immunomodulatory TGF-β and type-I interferon signaling pathways, respectively.
conclusionsOur study revealed both shared and distinct, cancer-promoting functions of PEVs, which contributed to the transcriptome and metastatic capabilities of the melanoma spheroids. Inhibiting the platelet receptors that modulate the PEVs' cancer-promoting properties may open up new strategies for identifying promising treatment targets for cancer therapy.
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