阿帕替尼对肺癌细胞侵袭和迁移的影响及其机制
[Effect of Apatinib on Invasion and Migration of Lung Cancer Cells and Its Mechanism].
作者信息
Yuan Yin, Gong Hao, Li Yongwen, Zhang Hongbing, Li Ying, Li Weiting, Wang Pan, Shi Ruifeng, Liu Hongyu, Chen Jun
机构信息
Department of Lung Cancer Surgery, Tianjin Medical University General Hospital, Tianjin 300052, China.
Tianjin Key Laboratory of lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin 300052, China.
出版信息
Zhongguo Fei Ai Za Zhi. 2019 May 20;22(5):264-270. doi: 10.3779/j.issn.1009-3419.2019.05.02.
BACKGROUND
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.
CONCLUSIONS
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.
背景
肺癌是全球对人类最致命的癌症之一。近年来，靶向治疗的效果日益显著。阿帕替尼是一种正在研究中的多靶点抗肿瘤药物。本研究旨在探讨阿帕替尼对肺癌细胞生物学特性的影响及其可能机制。
方法
体外培养肺癌细胞系H1299和H3255。采用细胞增殖实验、伤口愈合实验和Transwell实验检测阿帕替尼对H1299和H3255细胞增殖、迁移和侵袭的影响。通过蛋白质免疫印迹法检测与肿瘤血管生成和侵袭相关的蛋白表达。
结果
阿帕替尼以浓度依赖性方式显著抑制H1299和H3255细胞的增殖、迁移和侵袭。蛋白质免疫印迹法显示，随着药物浓度增加，血管内皮生长因子（VEGF）、血管内皮生长因子受体2（VEGFR2）、N-钙黏蛋白、基质金属蛋白酶9（MMP9）、基质金属蛋白酶2（MMP2）和波形蛋白表达下调，E-钙黏蛋白表达上调。
结论
阿帕替尼可抑制肺腺癌细胞H1299和H3255的侵袭和迁移，其机制可能与调控上皮-间质转化及基质金属蛋白酶相关蛋白表达有关。
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