Abstract
Tumor cell metastasis is a complex multistep process involving homotypic and heterotypic interactions among tumor cells and host cells (i. e. platelets, endothelial cells, etc.) in addition to tumor cell interactions with the extracellular matrix. These interactions are mediated by a variety of cell surface receptors including cadherins, CAMs, selectins, and integrins.1 To date a number of integrin receptors have been shown to be critically involved in tumor cell development and metastasis. Most of the integrin receptors recognize one or two matrix proteins (α5β1-fibronectin, α6β1-laminin and collagen).1,2 However, two members of the β3 integrin family, αIIbβ3 and αvβ3, recognize a large number of ECM proteins such as fibrinogen, fibronectin, vitronectin, thrombospondin, and von Willebrand factor.2 Cells expressing these receptors have an advantage to adhere to a variety of basement membrane proteins and thereby generate different matrix driven cellular responses.
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Trikha, M., Honn, K.V. (1997). Role of 12-Lipoxygenase and Protein Kinase C in Modulating the Activation State of the Integrin αIIbβ3 on Human Tumor Cells. In: Honn, K.V., Marnett, L.J., Nigam, S., Jones, R.L., Wong, P.YK. (eds) Eicosanoids and other Bioactive Lipids in Cancer, Inflammation, and Radiation Injury 3. Advances in Experimental Medicine and Biology, vol 407. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-1813-0_8
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DOI: https://doi.org/10.1007/978-1-4899-1813-0_8
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