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。
Background and objective Lung cancer is one of the most deadly cancers in the world for human. In recent years, the effect of targeted therapy has become increasingly significant. Apatinib is a multi-target anti-tumor drug that is currently under study. The purpose of this study is to investigate the effects of Apatinib on the biological characteristics of lung cancer cells and its possible mechanism. Methods Lung cancer cell lines H1299 and H3255 were cultured in vitro. The effects of Apatinib on proliferation, migration and invasion of H1299 and H3255 cells were detected by cell proliferation assays wound healing assays and Transwell assays. The protein expression related to cancer angiogenesis and invasion was detected by Western blot. Results Apatinib significantly inhibited the proliferation, migration and invasion of H1299 and H3255 in a concentration-dependent manner. Western blot showed that with the increasing of drug concentration, VEGF, VEGFR2, N-cadherin, MMP9, MMP2 and Vimentin were down-regulated, and E-cadherin were up-regulated. Conclusion Apatinib can inhibit the invasion and migration of lung adenocarcinoma cells H1299 and H3255. By regulation of epithelial-mesenchymal transition and the expression of matrix metalloproteinase-related proteins.
Chinese Journal of Lung Cancer