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Proteomics profiling identifies extracellular vesicles' cargo associated with tumour cell induced platelet
Niamh McNamee1,2,3, Laura Rodriguez de la Fuente1,2, Maria Jose Santos-Martinez1,2,4
1School of Pharmacy and Pharmaceutical Sciences, Trinity College Dublin, Dublin, Ireland.
BMC Cancer
|September 28, 2022
Summary
Triple-negative breast cancer cells and their extracellular vesicles (EVs) promote platelet aggregation. Researchers identified specific EV proteins that may offer new therapeutic targets for preventing thrombosis in cancer patients.
Area of Science:
- Oncology
- Hematology
- Cell Biology
Background:
- Cancer patients face a high risk of venous thromboembolism, a leading cause of mortality.
- Cancer cells can trigger platelet aggregation, contributing to thrombosis and metastasis.
- The role of cancer cell-derived extracellular vesicles (EVs) in platelet function remains underexplored.
Purpose of the Study:
- To investigate the impact of extracellular vesicles (EVs) from triple-negative breast cancer (TNBC) cells on platelet aggregation.
- To identify potential therapeutic targets within TNBC cell-derived EVs.
Main Methods:
- Separation and characterization of EVs from TNBC cell lines using filtration, ultracentrifugation, nanoparticle tracking analysis, immunoblots, and electron microscopy.
- Evaluation of platelet aggregation induced by TNBC cells and their EVs using light transmission aggregometry.
- Proteomic analysis of EV cargo via mass spectrometry to identify key proteins.
Main Results:
- Both TNBC cell variants and their released EVs significantly induced platelet aggregation.
- EV-induced platelet aggregation was dose-dependent.
- Proteomic analysis identified candidate proteins, including uPAR and PDGFRβ, within EVs that may mediate this effect.
Conclusions:
- Triple-negative breast cancer cells and their secreted EVs are potent inducers of platelet aggregation.
- Identified EV cargo proteins represent potential therapeutic targets for managing cancer-associated thrombosis.
