下调极光激酶A活性抑制Hep2细胞的促血管生成作用和迁移、侵袭能力

Down-regulation of aurora kinase A activity inhibits pro-angiogenesis, migration and invasion of Hep2 cells

目的·探索极光激酶A(aurora kinase A,AURKA)活性对人喉癌Hep2细胞促血管生成作用和迁移、侵袭能力的影响。方法·使用100 nmol/L的VX680下调Hep2细胞中AURKA磷酸化,Western blotting检测VX680作用于细胞0(空白对照)、24、48 h时磷酸化AURKA(p-AURKA)与血管内皮生长因子A(vascular endothelial growth factor A,VEGFA)及其受体VEGFR2蛋白表达情况。血管生成试验观察VX680对Hep2细胞促血管生成的影响。通过CCK8细胞增殖试验和Transwell细胞迁移、侵袭试验分别观察Hep2细胞增殖和迁移、侵袭能力。结果·与空白对照细胞相比,VX680作用48 h时p-AURKA蛋白表达水平降低(P=0.000)。下调p-AURKA后,VEGFA、VEGFR2蛋白表达水平降低(均P=0.000);同时,血管生成减少,Hep2细胞迁移、侵袭能力降低(均P=0.000)。结论·AURKA调控喉癌Hep2细胞的促血管生成作用及迁移、侵袭能力,以AURKA分子为药物治疗靶点可作为治疗喉癌的新策略。

Objective·To investigate the effect of aurora kinase A(AURKA)activity on pro-angiogenesis,migration and invasion of Hep2 cells.Methods·Down-regulation of AURKA phospholation in Hep2 cells with 100 nmol/L VX680.Western blotting was used to detect the expression of p-AURKA,vascular endothelial growth factor A(VEGFA)and its receptor VEGFR2 in blank control Hep2 cells and Hep2 cells treated with VX680 for 24 h and 48 h.Angiogenesis experiment was applied to observe the effect of Hep2 cells treated with VX680 on angiogenesis.CCK8 cell proliferation assay,Transwell migration and invasion experiment were used to observe the ability of cell proliferation,migration and invasion of Hep2 cells.Results·Compared with control cells,the expression of p-AURKA in Hep2 cells treated with VX680 for 48 h was decreased(P=0.000).After downregulation of p-AURKA,the expressions of VEGFA and VEGFR2 were decreased(P=0.000).Meanwhile,angiogenesis was inhibited(P=0.000),and migration and invasion of Hep2 cells were reduced(P=0.000).Conclusion·AURKA regulates pro-angiogenesis,migration and invasion of Hep2 cells,which is a new strategy for the treatment of laryngeal cancer by targeting AURKA.