Ouchani Farid, Jeanne Albin, Thevenard Jessica, Helesbeux Jean-Jacques, Wahart Amandine, Letinois Isabelle, Duval Olivier, Martiny Laurent, Charpentier Emmanuelle, Devy Jérôme
CNRS UMR7369 MEDyC, Laboratoire SiRMa, SFR CAP-Santé, Université de Reims Champagne-Ardenne, Moulin de la Housse, BP 1039, 51687, Reims cedex 2, France.
Invest New Drugs. 2015 Feb;33(1):75-85. doi: 10.1007/s10637-014-0184-4. Epub 2014 Nov 19.
Angiogenesis plays a pivotal role in tumorigenesis and also contributes to the pathogenesis of hematologic malignancies. A number of plant compounds have shown efficacy in preclinical and clinical studies and some of them possess an anti-angiogenic activity. Our present findings report anti-angiogenic activities of ethoxyfagaronine (etxfag), a synthetic derivative of fagaronine. Once determined the non-cytotoxic concentration of etxfag, we showed that the drug inhibits VEGF-induced angiogenesis in a Matrigel™ plug assay and suppresses ex vivo sprouting from VEGF-treated aortic rings. Each feature leading to neovascularization was then investigated and results demonstrate that etxfag prevents VEGF-induced migration and tube formation in human umbilical vein endothelial cells (HUVEC). Moreover, etxfag also suppresses VEGF-induced VEGFR-2 phosphorylation and inhibits FAK phosphorylation at Y-861 as well as focal adhesion complex turnover. Beside these effects, etxfag modifies MT1-MMP localization at the endothelial cell membrane. Finally, immunoprecipitation assay revealed that etxfag decreases VEGF binding to VEGFR-2. As we previously reported that etxfag is able to prevent leukemic cell invasiveness and adhesion to fibronectin, all together our data collectively support the anti-angiogenic activities of etxfag which could represent an additional approach to current anti-cancer therapies.
血管生成在肿瘤发生过程中起关键作用,也与血液系统恶性肿瘤的发病机制有关。许多植物化合物在临床前和临床研究中已显示出疗效,其中一些具有抗血管生成活性。我们目前的研究结果报告了法加罗宁的合成衍生物乙氧基法加罗宁(etxfag)的抗血管生成活性。一旦确定了etxfag的非细胞毒性浓度,我们发现在基质胶™ 塞试验中该药物抑制VEGF诱导的血管生成,并抑制VEGF处理的主动脉环的体外发芽。然后研究了导致新血管形成的每个特征,结果表明etxfag可防止人脐静脉内皮细胞(HUVEC)中VEGF诱导的迁移和管形成。此外,etxfag还抑制VEGF诱导的VEGFR-2磷酸化,并抑制Y-861处的FAK磷酸化以及粘着斑复合物的周转。除了这些作用外,etxfag还改变了MT1-MMP在内皮细胞膜上的定位。最后,免疫沉淀试验表明etxfag降低了VEGF与VEGFR-2的结合。正如我们之前报道的etxfag能够阻止白血病细胞的侵袭性和对纤连蛋白的粘附,我们所有的数据共同支持了etxfag的抗血管生成活性,这可能代表了当前抗癌治疗的另一种方法。