Murata J, Saiki I, Iida J, Azuma I, Kawahara H, Nishi N, Tokura S
Institute of Immunological Science, Hokkaido University, Sapporo, Japan.
Int J Biol Macromol. 1989 Aug;11(4):226-32. doi: 10.1016/0141-8130(89)90073-1.
Anti-cell adhesive activity was examined by the synthetic polypeptide, containing repetitive Arg-Gly-Asp sequence of cell attachment site from fibronectin, poly (Arg-Gly-Asp). The attachment of tumour cells to fibronectin substrate was specifically inhibited by adding poly (Arg-Gly-Asp) in cell surface receptor-mediated and divalent cation-dependent manners, but not by unrelated peptides. In our previous study, the lung metastatic formation of tumour cells was dramatically reduced by intravenous co-injection of anti-cell adhesive poly (Arg-Gly-Asp) with B16-BL6 melanoma cells. These findings suggest that polypeptide-mediated inhibition of pulmonary metastasis is partly due to interference with tumour cell adhesion to the substrates including fibronectin in target organs or tissues.
通过合成多肽聚(精氨酸 - 甘氨酸 - 天冬氨酸)(poly (Arg-Gly-Asp))检测抗细胞黏附活性,该多肽含有来自纤连蛋白的细胞附着位点的重复精氨酸 - 甘氨酸 - 天冬氨酸序列。通过以细胞表面受体介导和二价阳离子依赖的方式添加聚(精氨酸 - 甘氨酸 - 天冬氨酸),肿瘤细胞与纤连蛋白底物的附着受到特异性抑制,但不相关的肽则无此作用。在我们之前的研究中,通过将抗细胞黏附性的聚(精氨酸 - 甘氨酸 - 天冬氨酸)与B16 - BL6黑色素瘤细胞静脉共同注射,肿瘤细胞的肺转移形成显著减少。这些发现表明,多肽介导的肺转移抑制部分是由于干扰肿瘤细胞与包括靶器官或组织中的纤连蛋白在内的底物的黏附。