doi: 10.1161/ATVBAHA.108.176149
© 2008 American Heart Association, Inc.
Editorials |
Sharing Tissue Factor
A Winning Strategy in Tumorigenesis
From the Biomedical Research Division, The University of Texas Health Science Center at Tyler.
Correspondence to L. Vijaya Mohan Rao, Biomedical Research, The University of Texas Health Science Center at Tyler, 11937 US HWY 271, Tyler, TX 75708. E-mail Vijay.Rao@uthct.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Existence of a close relationship between increased clotting and malignancy has been clearly recognized for over a century. Many tumor cell types express tissue factor (TF), a procoagulant protein, on their cell surfaces. Tissue factor is a transmembrane cellular receptor for coagulation factor VII/VIIa. Binding of factor VIIa to TF triggers the activation of coagulation cascade leading ultimately to the generation of thrombin which in turn stimulates platelet activation and cleaves fibrinogen. Thus, there is no surprise that the activation of coagulation by tumor cell TF or by membrane fragments shed from tumor cells carrying TF contributes to cancer-associated thrombotic disorders.1,2 The close association between cancer and TF has also raised the possibility that TF may contribute to the pathogenesis of cancer beyond thrombosis. In fact, there are a number of reports in the literature showing that TF expressed by tumor cells plays an important role in both primary tumor growth and metastasis (see reviews3–5). The prometastatic effect of TF involves both activation of the coagulation pathway (eg, mechanisms linked to thrombin generated by TF) and effects mediated through the direct signaling activity of TF, probably via the cytoplasmic domain of TF.6 Recent studies have shown that direct TF-FVIIa protease-induced cell signaling is a major contributor to tumor growth in breast cancer.7 However, there are a couple of convincing reports in the literature that provide evidence that is contrary to the general belief that tumor-derived TF is crucial for primary tumor growth or metastasis. Toomey et al,8 using embryonic
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