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Blood, 15 February 2005, Vol. 105, No. 4, pp. 1734-1741.
Prepublished online as a Blood First Edition Paper on October 19, 2004; DOI 10.1182/blood-2004-05-2042.
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NEOPLASIA
Oncogenic events regulate tissue factor expression in colorectal cancer cells: implications for tumor progression and angiogenesis
Joanne L. Yu,
Linda May,
Vladimir Lhotak,
Siranoush Shahrzad,
Senji Shirasawa,
Jeffrey I. Weitz,
Brenda L. Coomber,
Nigel Mackman, and
Janusz W. Rak
From the Henderson Research Centre, Experimental Thrombosis Research, McMaster University, Hamilton, ON, Canada; Department of Biomedical Sciences, University of Guelph, Guelph, ON, Canada; Department of Pathology, International Medical Center of Japan, Tokyo, Japan; and Departments of Immunology and Vascular Biology, The Scripps Research Institute, La Jolla, CA.
Tissue factor (TF) is the primary cellular initiator of blood coagulation and a modulator of angiogenesis and metastasis in cancer. Indeed, systemic hypercoagulability in patients with cancer and TF overexpression by cancer cells are both closely associated with tumor progression, but their causes have been elusive. We now report that in human colorectal cancer cells, TF expression is under control of 2 major transforming events driving disease progression (activation of K-ras oncogene and inactivation of the p53 tumor suppressor), in a manner dependent on MEK/mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3'-kinase (PI3K). Furthermore, the levels of cell-associated as well as circulating (microvesicle-associated) TF activity are linked to the genetic status of cancer cells. Finally, RNA interference experiments suggest that TF expression is an important effector of the K-ras-dependent tumorigenic and angiogenic phenotype in vivo. Thus, this study establishes a causal link between cancer coagulopathy, angiogenesis, and genetic tumor progression. (Blood. 2005;105:1734-1741)
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