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首页> 外文期刊>Cellular Oncology: Analytical Cellular Pathology >Targeting Focal Adhesion Assembly by Ethoxyfagaronine Prevents Lymphoblastic Cell Adhesion to Fibronectin
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Targeting Focal Adhesion Assembly by Ethoxyfagaronine Prevents Lymphoblastic Cell Adhesion to Fibronectin

机译：乙氧基法加宁靶向局灶性粘连防止纤维母细胞淋巴母细胞粘连。

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Background: Leukemic cell adhesion to proteins of the bone marrow microenvironment provides signals which control morphology, motility and cell survival. We described herein the ability of ethoxyfagaronine (etxfag), a soluble synthetic derivative of fagaronine, to prevent leukemic cell adhesion to fibronectin peptide (FN/V).Methods: Phosphorylation of fak and pyk2 were evaluated by immunoblotting. Labelled proteins were localized by confocal microscopy. PI 3-kinase activity was evaluated byin vitrokinase assay.Results: Subtoxic concentration of etxfag reduced L1210 cell adhesion to FN/V dependently of β1 integrin engagement. Etxfag impaired FN-dependent formation of β1 clustering without modifying β1 expression at the cell membrane. This was accompanied by a decrease of focal adhesion number, a diminution of fak and pyk2 phosphorylation at Tyr-576, Tyr-861 and Tyr-579, respectively leading to their dissociations from β1 integrin and inhibition of PI 3-kinase activity. Etxfag also induced a cell retraction accompanied by a redistribution of phosphorylated fak and pyk2 in the perinuclear region and lipid raft relocalization.Conclusion: Through its anti-adhesive potential, etxfag, combined with conventional cytotoxic drugs could be potentially designed as a new anti-leukemic drug.
机译：背景：白血病细胞对骨髓微环境蛋白的粘附提供了控制形态，运动性和细胞存活的信号。我们在此描述了乙氧基法加隆宁（etxfag）（一种可合成的法加隆宁衍生物）预防白血病细胞粘附于纤连蛋白肽（FN / V）的能力。方法：通过免疫印迹评估了fak和pyk2的磷酸化。通过共聚焦显微镜定位标记的蛋白质。结果：依托法克的亚毒性浓度降低了L1210细胞对FN / V的粘附，这取决于β1整联蛋白的参与。 Etxfag损害了FN依赖性的β1簇形成，而没有改变细胞膜上的β1表达。这伴随着粘着斑数目的减少，Tyr-576，Tyr-861和Tyr-579的fak和pyk2磷酸化的减少，分别导致它们与β1整联蛋白解离和PI 3激酶活性的抑制。 Etxfag还可诱导细胞收缩，并伴随着磷酸化的Fak和pyk2在核周区域的重新分布以及脂质筏的重新定位。结论：etxfag的抗粘附潜力可与常规细胞毒性药物联合使用，有望被设计为一种新的抗白血病药物药品。

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