Honn K V, Menter D G, Onoda J M, Steinert B W, Diglio C A, Taylor J D, Sloane B F
Department of Biological Sciences, Wayne State University, Detroit, Michigan 48202.
Adv Prostaglandin Thromboxane Leukot Res. 1987;17B:981-5.
We have proposed that tumor cell induction of platelet aggregation facilitates tumor cell attachment to endothelium and that this attachment is limited by endogenous PGI2. We have developed an in vitro model to study tumor cell-platelet-endothelial cell interactions in which endothelial cells are grown on microcarrier beads. Untreated endothelial cells inhibit tumor cell-induced platelet aggregation, as well as tumor cell attachment to endothelial cells. Inhibition of endothelial cell PGI2 production by indomethacin obviates this inhibition.
我们已经提出，肿瘤细胞诱导血小板聚集有助于肿瘤细胞附着于内皮细胞，并且这种附着受到内源性前列环素（PGI2）的限制。我们开发了一种体外模型来研究肿瘤细胞 - 血小板 - 内皮细胞之间的相互作用，其中内皮细胞生长在微载体珠上。未经处理的内皮细胞会抑制肿瘤细胞诱导的血小板聚集以及肿瘤细胞与内皮细胞的附着。吲哚美辛抑制内皮细胞PGI2的产生可消除这种抑制作用。
