Chopra H, Timar J, Rong X, Grossi I M, Hatfield J S, Fligiel S E, Finch C A, Taylor J D, Honn K V
Department of Pathology, VA Medical Center, Allen Park, MI 48101.
Clin Exp Metastasis. 1992 Mar;10(2):125-37. doi: 10.1007/BF00114589.
In vitro tumor cell-platelet interaction was examined using B16 amelanotic (B16a) melanoma cells. These tumor cells express the alpha IIb beta 3-type cytoadhesin. Aggregation studies demonstrated that tumor cell surface alpha IIb beta 3 mediates the recognition of platelets since pretreatment of tumor cells with antibody against alpha IIb beta 3 prevents platelet-tumor cell interaction as well as platelet activation measured by aggregometry, platelet eicosanoid metabolism and ultrastructural analysis. In B16a cells, disruption of the microfilaments and intermediate filaments inhibits mobility of alpha IIb beta 3 on the cell surface. Microtubules do not play a role in receptor mobility, because B16a cells do not possess well-defined microtubules in interphase and colchicine does not affect receptor mobility. Disruption of microfilaments or intermediate filaments results in an inhibition of tumor cell-platelet interaction as evidenced by aggregometry studies and ultrastructural analysis. We suggest that platelet interaction with tumor cells begins with alpha IIb beta 3-mediated receptor recognition followed by not only platelet activation but also microfilament- and vimentin intermediate filament-dependent tumor cell activation.
利用B16无黑色素(B16a)黑色素瘤细胞检测体外肿瘤细胞与血小板的相互作用。这些肿瘤细胞表达αIIbβ3型细胞粘附素。聚集研究表明,肿瘤细胞表面的αIIbβ3介导血小板的识别,因为用抗αIIbβ3抗体预处理肿瘤细胞可阻止血小板与肿瘤细胞的相互作用以及通过聚集测定法、血小板类花生酸代谢和超微结构分析所测定的血小板活化。在B16a细胞中,微丝和中间丝的破坏会抑制αIIbβ3在细胞表面的移动性。微管在受体移动性中不起作用,因为B16a细胞在间期没有明确的微管,秋水仙碱也不影响受体移动性。微丝或中间丝的破坏会导致肿瘤细胞与血小板的相互作用受到抑制,这在聚集测定研究和超微结构分析中得到了证实。我们认为,血小板与肿瘤细胞的相互作用始于αIIbβ3介导的受体识别,随后不仅是血小板活化,而且是微丝和波形蛋白中间丝依赖性肿瘤细胞活化。