Role of Platelet-Derived Extracellular Vesicles in Cancer and Metastasis

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (10 July 2023) | Viewed by 2849

Special Issue Editors


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Guest Editor
Department of Neuroscience, Imaging and Clinical Sciences and Center for Advanced Studies and Technology (CAST), “G. d’Annunzio” University, School of Medicine, 66100 Chieti, Italy
Interests: platelets; colorectal cancer; metastasis; antiplatelet drugs; aspirin; P2Y12 antagonists; eicosanoids; extracellular vesicles; nonsteroidal anti-inflammatory agents (NSAIDs); lipidomics; lipidomics for biomarker development
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Guest Editor
Department of Systems Pharmacology and Translational Therapeutics, University of Pennsylvania, 3400 Civic Center Boulevard, Philadelphia, PA, USA
Interests: vascular biology; pharmacology of nonsteroidal anti-inflammatory drugs; system pharmacology; genomics; metabolomics; microbiome; RNA-sequencing; atherosclerosis; heart failure; myocardial infarction; thrombosis; platelet aggregation; NSAID-induced enteropathy; aspirin and cancer

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Guest Editor
Department of Neuroscience, Imaging and Clinical Sciences, “G.d’Annunzio” University, 66100 Chieti, Italy
Interests: platelet; lipoxygenase; aspirin; platelet-derived microparticles; metastasis; cell–cell communication; inflammation; fibrosis

Special Issue Information

Dear Colleagues,

Platelets contribute to several types of cancer through many mechanisms. Platelets contain a changing repertoire of proteins and genetic material, including transcripts and microRNAs (i.e., small noncoding RNAs) that act as regulators of gene expression by post-transcriptional mechanisms. Upon platelet activation, biologically active molecules are secreted in a soluble form or packaged into extracellular vesicles (EVs). EVs have the peculiarity of interacting with cancer cells to transfer their molecular cargo. Moreover, EVs can activate other cells, including vascular and immune cells and fibroblasts. Hence, platelets are a crucial component of cell–cell communication, promoting tumorigenesis. In particular, their interaction with cancer cells can enhance their malignancy and facilitate the invasion and colonization of distant organs. These findings suggest the use of antiplatelet agents to restrain cancer development and progression. Another peculiarity of platelets is their ability to uptake proteins and transcripts from the circulation. Thus, cancer-patient platelets and platelet-derived EVs show specific proteomic and transcriptomic expression patterns, a phenomenon called tumor-educated platelets (TEPs). The transcriptomic/proteomic profile of platelets and EVs can provide early cancer detection and disease monitoring information.

This topic aims to highlight the latest advances in novel functions of EVs in cancer and metastasis development. Moreover, studies on the development of novel biomarkers based on the analysis of platelets and EVs for the early detection of cancer, as well as those on monitoring the disease and therapeutic efficacy, are of interest. Original research papers and review articles are welcomed.

We look forward to receiving your contributions.

Prof. Dr. Paola Patrignani
Dr. Emanuela Ricciotti
Dr. Annalisa Contursi
Guest Editors

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Keywords

  • extracellular vesicles
  • EVs
  • cancer
  • metastasis
  • platelets
  • antiplatelet drugs
  • lipidomics
  • platelet-derived microparticles
  • nonsteroidal anti-inflammatory agents (NSAIDs)

Published Papers (1 paper)

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Research

22 pages, 5229 KiB  
Article
Tumor-Educated Platelet Extracellular Vesicles: Proteomic Profiling and Crosstalk with Colorectal Cancer Cells
by Annalisa Contursi, Rosa Fullone, Paulina Szklanna-Koszalinska, Simone Marcone, Paola Lanuti, Francesco Taus, Alessandra Meneguzzi, Giulia Turri, Melania Dovizio, Annalisa Bruno, Corrado Pedrazzani, Stefania Tacconelli, Marco Marchisio, Patrizia Ballerini, Pietro Minuz, Patricia Maguire and Paola Patrignani
Cancers 2023, 15(2), 350; https://doi.org/10.3390/cancers15020350 - 5 Jan 2023
Cited by 6 | Viewed by 2325
Abstract
Background: Platelet–cancer cell interactions modulate tumor metastasis and thrombosis in cancer. Platelet-derived extracellular vesicles (EVs) can contribute to these outcomes. Methods: We characterized the medium-sized EVs (mEVs) released by thrombin-stimulated platelets of colorectal cancer (CRC) patients and healthy subjects (HS) on the capacity [...] Read more.
Background: Platelet–cancer cell interactions modulate tumor metastasis and thrombosis in cancer. Platelet-derived extracellular vesicles (EVs) can contribute to these outcomes. Methods: We characterized the medium-sized EVs (mEVs) released by thrombin-stimulated platelets of colorectal cancer (CRC) patients and healthy subjects (HS) on the capacity to induce epithelial-mesenchymal transition (EMT)-related genes and cyclooxygenase (COX)-2(PTGS2), and thromboxane (TX)B2 production in cocultures with four colorectal cancer cell lines. Platelet-derived mEVs were assessed for their size distribution and proteomics signature. Results: The mEV population released from thrombin-activated platelets of CRC patients had a different size distribution vs. HS. Platelet-derived mEVs from CRC patients, but not from HS, upregulated EMT marker genes, such as TWIST1 and VIM, and downregulated CDH1. PTGS2 was also upregulated. In cocultures of platelet-derived mEVs with cancer cells, TXB2 generation was enhanced. The proteomics profile of mEVs released from activated platelets of CRC patients revealed that 119 proteins were downregulated and 89 upregulated vs. HS. Conclusions: We show that mEVs released from thrombin-activated platelets of CRC patients have distinct features (size distribution and proteomics cargo) vs. HS and promote prometastatic and prothrombotic phenotypes in cancer cells. The analysis of platelet-derived mEVs from CRC patients could provide valuable information for developing an appropriate treatment plan. Full article
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