Heinmöller E, Schropp T, Kisker O, Simon B, Seitz R, Weinel R J
Dept. of Surgery, University Hospital, Philipps University Marburg, Germany.
Scand J Gastroenterol. 1995 Oct;30(10):1008-16. doi: 10.3109/00365529509096346.
Tumor cell-induced platelet aggregation (TCIPA) is considered to be a critical step in hematogenous metastasis.
TCIPA was studied in vitro in six human pancreatic carcinoma cell lines (PC 3, PC 44, AsPC1, BxPC3, Capan2, Panc1).
Whereas all cell lines induced aggregation of washed platelets in the presence of minimal amounts of platelet-poor plasma, five cell lines also induced aggregation of platelets in platelet-rich plasma. The thrombin-antagonist hirudin inhibited TCIPA in all cell lines indicating that TCIPA is thrombin-dependent. Since pretreatment of tumor cells with phospholipase A2 or C inhibited TCIPA, the thrombin-generating activity might be confined to the tumor cell surface. Further support for a prothrombinase activity was provided by the observation that all cell lines were able to induce the aggregation of washed platelets after addition of purified coagulation factors II and V.
Pancreatic carcinoma cells are able to induce platelet aggregation via activation of thrombin. This might support metastasis in pancreatic cancer and possibly explain the incidence of thrombosis in this tumor.
肿瘤细胞诱导的血小板聚集(TCIPA)被认为是血行转移的关键步骤。
在六种人胰腺癌细胞系(PC 3、PC 44、AsPC1、BxPC3、Capan2、Panc1)中对TCIPA进行体外研究。
虽然所有细胞系在存在少量贫血小板血浆的情况下均能诱导洗涤后血小板的聚集,但五种细胞系在富血小板血浆中也能诱导血小板聚集。凝血酶拮抗剂水蛭素抑制了所有细胞系中的TCIPA,表明TCIPA是凝血酶依赖性的。由于用磷脂酶A2或C预处理肿瘤细胞可抑制TCIPA,因此凝血酶生成活性可能局限于肿瘤细胞表面。所有细胞系在添加纯化的凝血因子II和V后均能诱导洗涤后血小板的聚集,这一观察结果进一步支持了凝血酶原酶活性。
胰腺癌细胞能够通过激活凝血酶诱导血小板聚集。这可能促进胰腺癌的转移,并可能解释该肿瘤中血栓形成的发生率。