Abdel-Ghany M, Cheng H, Levine R A, Pauli B U
Cancer Biology Laboratories, Department of Molecular Medicine, Cornell University College of Veterinary Medicine, Ithaca, NY 14853, USA.
Invasion Metastasis. 1998;18(1):35-43. doi: 10.1159/000024497.
A novel adhesion receptor/ligand pair was shown recently to mediate lung vascular arrest and metastasis of rat breast cancer cells. The interacting adhesion molecules are endothelial dipeptidyl peptidase IV (DPP IV) and tumor cell surface-associated, polymeric fibronectin (FN). A truncated DPP IV (DPP IV(31-767): amino acids 31-767) in which the FN-binding site is preserved is shown here to mask the breast cancer cell surface-associated FN complexes, causing a dose-dependent inhibition of adhesion to endothelial DPP IV and impeding lung colony formation by approximately 80%. Since surface accumulation of FN is chiefly occurring during dissemination in the blood and since many cancer cell types have surface receptors by which they may initiate FN accumulation on their surfaces, the present anti-metastatic treatment modality may extend its efficacy farther than appreciated by this study.
最近发现一种新型黏附受体/配体对可介导大鼠乳腺癌细胞的肺血管停滞和转移。相互作用的黏附分子是内皮二肽基肽酶IV(DPP IV)和肿瘤细胞表面相关的聚合纤连蛋白(FN)。本文显示,保留了FN结合位点的截短型DPP IV(DPP IV(31 - 767):氨基酸31 - 767)可掩盖乳腺癌细胞表面相关的FN复合物,导致对内皮DPP IV黏附的剂量依赖性抑制,并使肺集落形成减少约80%。由于FN的表面积累主要发生在血液传播过程中,且许多癌细胞类型具有可启动其表面FN积累的表面受体,因此目前的抗转移治疗方式可能比本研究所认识到的具有更远的疗效。