AN INDUCIBLE ENDOTHELIAL-CELL SURFACE GLYCOPROTEIN MEDIATES MELANOMA ADHESION
AN INDUCIBLE ENDOTHELIAL-CELL SURFACE GLYCOPROTEIN MEDIATES MELANOMA ADHESION
复制标题
DOI：
10.1126/science.2588007
复制
发表时间：
1989-12-08
期刊：
影响因子：
56.9
通讯作者：
BEVILACQUA, MP
中科院分区：
文献类型：
--
作者：
RICE, GE;BEVILACQUA, MP
血行转移需要血源性肿瘤细胞的滞留和渗出，这可能涉及与血管内皮的直接黏附相互作用。培养的人内皮细胞经细胞因子激活后，会增加黑色素瘤和癌细胞系的黏附。一种可诱导的110 - kD内皮细胞表面糖蛋白，被命名为INCAM - 110，似乎介导黑色素瘤细胞的黏附。此外，一种可诱导的中性粒细胞内皮受体ELAM - 1，支持一种人结肠癌细胞系的黏附。因此，体内血管内皮的激活导致INCAM - 110和ELAM - 1表达增加，可能促进肿瘤细胞黏附，并影响转移的发生率和分布。
Hematogenous metastasis requires the arrest and extravasation of blood-borne tumor cells, possibly involving direct adhesive interactions with vascular endothelium. Cytokine activation of cultured human endothelium increases adhesion of melanoma and carcinoma cell lines. An inducible 110-kD endothelial cell surface glycoprotein, designated INCAM-110, appears to mediate adhesion of melanoma cells. In addition, an inducible endothelial receptor for neutrophils, ELAM-1, supports the adhesion of a human colon carcinoma cell line. Thus, activation of vascular endothelium in vivo that results in increased expression of INCAM-110 and ELAM-1 may promote tumor cell adhesion and affect the incidence and distribution of metastases.