Contribution of platelets to tumour metastasis.
TLDR
Contributions of platelets to tumour cell survival and spread suggest platelets as a new avenue for therapy.Abstract:
Experimental evidence suggests that platelets contribute to metastasis through adhesive and haemostatic functions that promote cancer cell survival, immune evasion and interactions with vascular cells to assist organ colonization from the bloodstream. Extensive experimental evidence shows that platelets support tumour metastasis. The activation of platelets and the coagulation system have a crucial role in the progression of cancer. Within the circulatory system, platelets guard tumour cells from immune elimination and promote their arrest at the endothelium, supporting the establishment of secondary lesions. These contributions of platelets to tumour cell survival and spread suggest platelets as a new avenue for therapy.read more
Citations
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Journal ArticleDOI
Microenvironmental regulation of tumor progression and metastasis.
TL;DR: The paradoxical roles of the tumor microenvironment during specific stages of cancer progression and metastasis are discussed, as well as recent therapeutic attempts to re-educate stromal cells within the TME to have anti-tumorigenic effects.
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Emerging Biological Principles of Metastasis
TL;DR: The cellular and molecular mechanisms involved in metastasis are summarized, with a focus on carcinomas where the most is known, and the general principles of metastasis that have begun to emerge are highlighted.
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Direct Signaling between Platelets and Cancer Cells Induces an Epithelial-Mesenchymal-Like Transition and Promotes Metastasis
TL;DR: It is shown that platelet-tumor cell interactions are sufficient to prime tumor cells for subsequent metastasis and inhibit NF-κB signaling in cancer cells, resulting in their transition to an invasive mesenchymal-like phenotype and enhanced metastasis in vivo.
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Pre-metastatic niches: organ-specific homes for metastases
Héctor Peinado,Haiying Zhang,Irina Matei,Bruno Costa-Silva,Ayuko Hoshino,Gonçalo Rodrigues,Gonçalo Rodrigues,Bethan Psaila,Rosandra N. Kaplan,Jacqueline Bromberg,Yibin Kang,Mina J. Bissell,Thomas R. Cox,Amato J. Giaccia,Janine T. Erler,Sachie Hiratsuka,Cyrus M. Ghajar,David Lyden,David Lyden +18 more
TL;DR: This Review summarizes the main processes and new mechanisms involved in the formation of the pre-metastatic niche and describes the main mechanisms used to modify organs of future metastasis.
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The physics of cancer: the role of physical interactions and mechanical forces in metastasis
TL;DR: The metastatic process is reconstructed and the importance of key physical and mechanical processes at each step of the cascade is described, which may help to solve some long-standing questions in disease progression and lead to new approaches to developing cancer diagnostics and therapies.
References
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Adhesion Mechanisms in Platelet Function
TL;DR: The results obtained now permit an attempt to integrate all the available information into a picture that highlights the balanced diversity and synergy of distinct platelet adhesive interactions.
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Integrin activation controls metastasis in human breast cancer
Brunhilde Felding-Habermann,Timothy E. O'Toole,Jeffrey W. Smith,Emilia Fransvea,Zaverio M. Ruggeri,Mark H. Ginsberg,Paul E. Hughes,Nisar A. Pampori,Sanford J. Shattil,Alan Saven,Barbara M. Mueller +10 more
TL;DR: It is shown that integrin alpha v beta 3 supports breast cancer cell attachment under blood flow conditions in an activation-dependent manner and alterations within tumors that lead to the aberrant control of integrin activation are expected to adversely affect the course of human breast cancer.
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Fibrinogen is an important determinant of the metastatic potential of circulating tumor cells.
Joseph S. Palumbo,Keith W. Kombrinck,Angela F. Drew,Timothy S. Grimes,John H. Kiser,Jay L. Degen,Thomas H. Bugge +6 more
TL;DR: It is concluded that fibrin(ogen) is a critical determinant of the metastatic potential of circulating tumor cells and thrombin appears to facilitate tumor dissemination through at least one fibrIn(ogen)-independent mechanism.
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Defective platelet activation in G alpha q deficient mice
TL;DR: It is shown that platelets from mice deficient in the α-subunit of the heterotrimeric guanine-nucleotide-binding protein Gq are unresponsive to a variety of physiological platelet activators, and that Gαq is essential for the signalling processes used by different platelet Activators and that it cannot be replaced by Gαi or the βγ subunits of the homophobic G proteins.
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Integrin Structure, Allostery, and Bidirectional Signaling
TL;DR: Newer NMR, crystallographic, and EM data, reviewed here, are providing a better picture of the dynamic integrin structure and the allosteric changes that guide its diverse functions.