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Human Cancer and Platelet Interaction, a Potential Therapeutic Target

Cancer patients experience a four-fold increase in thrombosis risk, indicating that cancer development and progression are associated with platelet activation. Xenograft experiments and transgenic mouse models further demonstrate that platelet activation and platelet-cancer cell interaction are cruc...

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Detalles Bibliográficos
Autores principales: Wang, Shike, Li, Zhenyu, Xu, Ren
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5979598/
https://www.ncbi.nlm.nih.gov/pubmed/29677116
http://dx.doi.org/10.3390/ijms19041246
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author Wang, Shike
Li, Zhenyu
Xu, Ren
author_facet Wang, Shike
Li, Zhenyu
Xu, Ren
author_sort Wang, Shike
collection PubMed
description Cancer patients experience a four-fold increase in thrombosis risk, indicating that cancer development and progression are associated with platelet activation. Xenograft experiments and transgenic mouse models further demonstrate that platelet activation and platelet-cancer cell interaction are crucial for cancer metastasis. Direct or indirect interaction of platelets induces cancer cell plasticity and enhances survival and extravasation of circulating cancer cells during dissemination. In vivo and in vitro experiments also demonstrate that cancer cells induce platelet aggregation, suggesting that platelet-cancer interaction is bidirectional. Therefore, understanding how platelets crosstalk with cancer cells may identify potential strategies to inhibit cancer metastasis and to reduce cancer-related thrombosis. Here, we discuss the potential function of platelets in regulating cancer progression and summarize the factors and signaling pathways that mediate the cancer cell-platelet interaction.
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spelling pubmed-59795982018-06-10 Human Cancer and Platelet Interaction, a Potential Therapeutic Target Wang, Shike Li, Zhenyu Xu, Ren Int J Mol Sci Review Cancer patients experience a four-fold increase in thrombosis risk, indicating that cancer development and progression are associated with platelet activation. Xenograft experiments and transgenic mouse models further demonstrate that platelet activation and platelet-cancer cell interaction are crucial for cancer metastasis. Direct or indirect interaction of platelets induces cancer cell plasticity and enhances survival and extravasation of circulating cancer cells during dissemination. In vivo and in vitro experiments also demonstrate that cancer cells induce platelet aggregation, suggesting that platelet-cancer interaction is bidirectional. Therefore, understanding how platelets crosstalk with cancer cells may identify potential strategies to inhibit cancer metastasis and to reduce cancer-related thrombosis. Here, we discuss the potential function of platelets in regulating cancer progression and summarize the factors and signaling pathways that mediate the cancer cell-platelet interaction. MDPI 2018-04-20 /pmc/articles/PMC5979598/ /pubmed/29677116 http://dx.doi.org/10.3390/ijms19041246 Text en © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Wang, Shike
Li, Zhenyu
Xu, Ren
Human Cancer and Platelet Interaction, a Potential Therapeutic Target
title Human Cancer and Platelet Interaction, a Potential Therapeutic Target
title_full Human Cancer and Platelet Interaction, a Potential Therapeutic Target
title_fullStr Human Cancer and Platelet Interaction, a Potential Therapeutic Target
title_full_unstemmed Human Cancer and Platelet Interaction, a Potential Therapeutic Target
title_short Human Cancer and Platelet Interaction, a Potential Therapeutic Target
title_sort human cancer and platelet interaction, a potential therapeutic target
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5979598/
https://www.ncbi.nlm.nih.gov/pubmed/29677116
http://dx.doi.org/10.3390/ijms19041246
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