Donati M B, Roncaglioni M C, Falanga A, Casali B, Semeraro N
Haemostasis. 1986;16(3-4):288-94. doi: 10.1159/000215300.
Anticoagulants of the coumarin type have long been reported to inhibit metastasis growth in experimental animals; however, the mechanisms of such effects has not been clarified. Systemic anticoagulation per se does not appear to account completely for such metastasis growth depression. More recent information gathered on a cell procoagulant activity, which is vitamin K-dependent, could probably supply a fresh insight into this problem. Indeed, vitamin K deficiency induced either dietarily or pharmacologically by warfarin, does inhibit the activity of a cysteine protease with direct factor-X-activating properties. This protease is only present in warfarin-sensitive tumors. The correlation of this activity with cancer cell invasiveness is supported by experimental data in metastatic variants and, lately, also by the observation of markedly higher cancer procoagulant activity in extracts from metastases than from primary human melanomas.
长期以来，有报道称香豆素类抗凝剂可抑制实验动物体内转移瘤的生长；然而，此类作用的机制尚未阐明。全身抗凝本身似乎并不能完全解释转移瘤生长受抑制的现象。最近收集到的关于一种维生素K依赖性细胞促凝活性的信息，可能会为这个问题提供新的见解。事实上，通过饮食或华法林药物诱导的维生素K缺乏，确实会抑制具有直接激活因子X特性的半胱氨酸蛋白酶的活性。这种蛋白酶仅存在于对华法林敏感的肿瘤中。转移变体的实验数据支持了这种活性与癌细胞侵袭性之间的相关性，最近，也有观察表明，转移灶提取物中的癌促凝活性明显高于原发性人类黑色素瘤提取物。
