F4, a collagen XIX-derived peptide, inhibits tumor angiogenesis through αvβ3 and α5β1 integrin interaction.

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC
Jean-Baptiste Oudart, Matthieu Villemin, Bertrand Brassart, Christèle Sellier, Christine Terryn, Aurélie Dupont-Deshorgue, Jean Claude Monboisse, François-Xavier Maquart, Laurent Ramont, Sylvie Brassart-Pasco
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引用次数: 2

Abstract

We previously demonstrated that F4 peptide (CNPEDCLYPVSHAHQR) from collagen XIX was able to inhibit melanoma cell migrationin vitro and cancer progression in a mouse melanoma model. The aim of the present work was to study the anti-angiogenic properties of F4 peptide. We demonstrated that F4 peptide inhibited VEGF-induced pseudo-tube formation on Matrigel by endothelial cells and endothelial sprouting in a rat aortic ring assay. By affinity chromatography, we identified αvβ3 and α5β1 integrins as potential receptors for F4 peptide on endothelial cell surface. Using solid phase assays, we proved the direct interaction between F4 and both integrins. Taken together, our results demonstrate that F4 peptide is a potent antitumor agent inhibiting both angiogenesis and tumor cell migration.

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Abstract Image

Abstract Image

F4是一种胶原衍生肽,通过αvβ3和α5β1整合素相互作用抑制肿瘤血管生成。
我们之前证明了来自XIX胶原的F4肽(CNPEDCLYPVSHAHQR)能够在体外抑制黑色素瘤细胞的迁移和小鼠黑色素瘤模型中的癌症进展。本研究的目的是研究F4肽的抗血管生成特性。我们在大鼠主动脉环实验中通过内皮细胞和内皮发芽证明了F4肽抑制vegf诱导的Matrigel伪管形成。通过亲和层析,我们发现αvβ3和α5β1整合素是内皮细胞表面F4肽的潜在受体。通过固相分析,我们证实了F4与这两种整合素之间的直接相互作用。综上所述,我们的研究结果表明F4肽是一种有效的抗肿瘤药物,可以抑制血管生成和肿瘤细胞的迁移。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
7.20
自引率
4.30%
发文量
567
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