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首页> 外文期刊>International journal of molecular medicine >Salinomycin exhibits anti-angiogenic activity against human glioma in vitro and in vivo by suppressing the VEGF-VEGFR2-AKT/FAK signaling axis
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Salinomycin exhibits anti-angiogenic activity against human glioma in vitro and in vivo by suppressing the VEGF-VEGFR2-AKT/FAK signaling axis

机译：沙利霉素通过抑制VEGF-VEGFR2-AKT / FAK信号轴在体外和体内对人神经胶质瘤表现出抗血管生成活性

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Tumor angiogenesis plays a crucial role in tumor growth, progression and metastasis, and suppression of tumor angiogenesis has been considered as a promising anticancer strategy. Salinomycin?(SAL), an antibiotic, displays novel anticancer potential against several human cancer cells in?vitro and in?vivo. However, little information concerning its anti-angiogenic properties is available. Therefore, the anti?angiogenic effect of SAL and the underlying mechanism in human glioma were evaluated in the present study. The results indicated that SAL treatment significantly inhibited human umbilical vein endothelial cell?(HUVEC) proliferation, migration, invasion and capillary-like tube formation. Further investigation on intracellular mechanisms showed that SAL markedly suppressed FAK and AKT phosphorylation, and downregulated vascular endothelial growth factor?(VEGF) expression in HUVECs. Pretreatment of cells with a PI3K inhibitor (LY294002) and FAK inhibitor (PF562271) markedly enhanced SAL-induced inhibition of HUVEC proliferation and migration, respectively. Moreover, U251 human glioma xenograft growth was also effectively blocked by SAL treatment in?vivo via inhibition of angiogenesis involving FAK and AKT depho-sphorylation. Taken together, our findings validated that SAL inhibits angiogenesis and human glioma growth through suppression of the VEGF-VEGFR2-AKT/FAK signaling axis, indicating the potential application of SAL for the treatment of human glioma.
机译：肿瘤血管生成在肿瘤生长，进展和转移中起关键作用，抑制肿瘤血管生成已被认为是一种有前途的抗癌策略。 Salinomycin？（SAL）是一种抗生素，在体外和体内对几种人类癌细胞均显示出新的抗癌潜力。然而，关于其抗血管生成特性的信息很少。因此，本研究评估了SAL的抗血管生成作用及其在人脑胶质瘤中的潜在机制。结果表明，SAL治疗可显着抑制人脐静脉内皮细胞（HUVEC）的增殖，迁移，侵袭和毛细血管样管形成。对细胞内机制的进一步研究表明，SAL可以显着抑制HUVEC中的FAK和AKT磷酸化，并下调血管内皮生长因子（VEGF）的表达。用PI3K抑制剂（LY294002）和FAK抑制剂（PF562271）预处理细胞分别显着增强了SAL对HUVEC增殖和迁移的抑制作用。此外，通过抑制涉及FAK和AKT磷酸化的血管生成，还可以在体内通过SAL治疗有效阻断U251人神经胶质瘤异种移植物的生长。综上所述，我们的发现验证了SAL通过抑制VEGF-VEGFR2-AKT / FAK信号转导轴抑制了血管生成和人类神经胶质瘤的生长，表明SAL在治疗人类神经胶质瘤中的潜在应用。

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