Abstract
背景与目的肺癌是世界上对人类健康产生重大危害的癌症之一，近年来靶向治疗的效果日益显著。阿帕替尼（Apatinib, YN968D1）是目前研究较热的多靶点抗肿瘤药物，本研究旨在探讨Apatinib对肺癌细胞生物学特性的影响和其可能的作用机制。方法体外培养肺腺癌细胞株H1299与H3255，CCK法、划痕实验及Transwell实验检测Apatinib对H1299与H3255细胞增殖、迁移及侵袭的影响，Western blot检测肿瘤血管生成和侵袭相关蛋白的表达。结果Apatinib显著抑制H1299与H3255的增殖、迁移及侵袭能力，并呈浓度依赖性。Western blot显示，随药物浓度增加，VEGF、VEGFR2、N-cadherin、MMP9、MMP2、Vimentin表达下调，E-cadherin表达上调。结论Apatinib可抑制肺腺癌细胞H1299、H3255的侵袭迁移能力，其机制可能通过调控上皮-间充质转化及基质金属蛋白酶相关蛋白的表达来实现。
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