Tissue factor isoforms in cancer and coagulation: May the best isoform win


Kocaturk B. , Versteeg H. H.

THROMBOSIS RESEARCH, vol.129, 2012 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 129
  • Publication Date: 2012
  • Doi Number: 10.1016/s0049-3848(12)70020-8
  • Title of Journal : THROMBOSIS RESEARCH
  • Keywords: Tissue factor, Splicing, Blood clotting, Tumor, Thrombosis, FACTOR CYTOPLASMIC DOMAIN, HUMAN-ENDOTHELIAL-CELLS, PROTEASE-ACTIVATED RECEPTOR-1, FACTOR EXPRESSION, TUMOR-CELLS, FACTOR VIIA, BREAST-CANCER, INDEPENDENT MECHANISMS, PANCREATIC-CANCER, PROGNOSTIC-FACTOR

Abstract

Tissue factor (TF), the trigger of blood coagulation, is a 47 kDa membrane protein that also impacts on non-hemostatic processes, such as atherosclerosis, primary tumor growth and metastasis. TF binding to its ligand FVIIa induces activation of protease-activated receptor-2 and this event is thought to considerably influence atherosclerosis and tumor angiogenesis. TF-dependent activation of the coagulation cascade, rather than PAR-2 activation, then leads to the potentiation of metastasis. Importantly, a soluble alternatively spliced isoform of TF (asTF) has been discovered, but the function of asTF in hemostatic and non-hemostatic events is poorly understood. In this review, we aim to present a side-by-side evaluation of normally-spliced, full length TF (flTF) and asTF with regard to coagulant function, atherosclerosis, tumor progression and malignancy-associated thrombosis. (C) 2012 Elsevier Ltd. All rights reserved.