摘要/Abstract

摘要： 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（ P0.000）。下调 p-AURKA后，VEGFA、VEGFR2蛋白表达水平降低（均 P0.000）；同时，血管生成减少， Hep2细胞迁移、侵袭能力降低（均 P0.000）。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。
关键词: 头颈鳞状细胞癌, 极光激酶 A, 血管生成, 迁移, 侵袭
Abstract:
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 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 of p-AURKA in Hep2 cells treated with VX680 for 48 h was decreased (P0.000). After down-regulation of p-AURKA, the s of VEGFA and VEGFR2 were decreased (P0.000). Meanwhile, angiogenesis was inhibited (P0.000), and migration and invasion of Hep2 cells were reduced (P0.000). Conclusion · AURKA regulates pro-angiogenesis, migration and invasion of Hep2 cells, which is a new strategy for the treatment of laryngeal cancertargeting AURKA.
Key words: head and neck squamous cell carcinoma, aurora kinase A (AURKA), angiogenesis, migration, invasion


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