截断二肽基肽酶IV是一种有效的抗乳腺癌细胞粘附和转移肽。

M Abdel-Ghany, H Cheng, R A Levine, B U Pauli
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引用次数: 31

摘要

最近发现一种新的粘附受体/配体对介导大鼠乳腺癌细胞肺血管阻滞和转移。相互作用的粘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维连接蛋白(FN)。截断的DPP IV(DPP IV(31-767):氨基酸31-767)保留了FN结合位点,可以掩盖乳腺癌细胞表面相关的FN复合物,导致对内皮细胞DPP IV粘附的剂量依赖性抑制,并阻碍肺集落形成约80%。由于FN的表面积累主要发生在血液传播过程中,并且由于许多癌细胞类型具有表面受体,它们可以通过表面受体启动FN在其表面的积累,因此目前的抗转移治疗方式可能比本研究所认识到的更有效。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Truncated dipeptidyl peptidase IV is a potent anti-adhesion and anti-metastasis peptide for rat breast cancer cells.
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.
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