Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037, USA.
Thromb Res. 2012 Apr;129 Suppl 1:S127-31. doi: 10.1016/S0049-3848(12)70032-4.
Cancer progression from a dormant, non-vascularized benign tumor to metastatic disease is a multiple steps process that critically depends on contributions from the hemostatic system. Tissue factor (TF), protease activated receptors (PARs), factor VIIa, and the endothelial protein C receptor (EPCR) are expressed by tumor cells as well as the host compartment. These components of the hemostatic system regulate tumor growth, angiogenesis and metastasis. Here we review the evidence that TF-dependent signaling is the major driver of primary tumor growth, whereas TF-initiated coagulation and interactions of procoagulant tumor cells with the host compartments initiate multiple pathways that support and regulate the efficiency of metastatic tumor dissemination.
癌症从休眠、非血管化的良性肿瘤发展为转移性疾病是一个多步骤的过程，严重依赖于止血系统的贡献。组织因子 (TF)、蛋白酶激活受体 (PARs)、因子 VIIa 和内皮蛋白 C 受体 (EPCR) 不仅由肿瘤细胞表达，也由宿主细胞表达。这些止血系统的组成部分调节肿瘤生长、血管生成和转移。在这里，我们回顾了证据表明 TF 依赖性信号是原发性肿瘤生长的主要驱动因素，而 TF 引发的凝血和促凝肿瘤细胞与宿主细胞间的相互作用则启动了多种支持和调节转移性肿瘤扩散效率的途径。
