【摘要】 目的 探究安罗替尼对人脑胶质瘤细胞黏附、迁移、侵袭和上皮间质转化（EMT）的影响。方法 体外培养人脑胶质瘤T98G细胞，分为对照组（不做干预）、实验组(2.5μmol·L^-1安罗替尼组、5μmol·L^-1安罗替尼组、10μmol·L^-1安罗替尼组)和阳性药物组(50 mg·L^-1 5-氟尿嘧啶),干预24 h。用活细胞计数（CCK-8）、细胞黏附实验、划痕法、Transwell小室及蛋白免疫印迹（WB）法对细胞增殖活力、黏附、迁移、侵袭能力及EMT相关蛋白表达量进行分析。结果 与对照组比较，5μmol·L^-1、10μmol·L^-1安罗替尼组和阳性药物组增殖活力显著降低（P<0.05）,实验组和阳性药物组T98G细胞黏附、迁移、侵袭能力，纤维粘连蛋白（FN）、波形蛋白（Vimentin）、N-钙黏蛋白（N-cadherin）蛋白的表达水平呈现显著下调趋势（P<0.05）,而E-钙黏蛋白（E-cadherin）蛋白的表达水平呈现明显上调趋势（P<0.05）,且浓度越高变化越显著；与阳性药物组相比，2.5μmol·L^-1、5μmol·L^-1安罗替尼组细胞增殖活力、黏附、迁移、侵袭能力，N-cadherin、Vimentin及FN的蛋白水平上调（P<0.05）,而E-cadherin蛋白水平则下调（P<0.05）;10μmol·L^-1安罗替尼组与阳性药物组相比无显著差异（P>0.05）。结论 安罗替尼可能是通过抑制EMT进程进而抑制人脑胶质瘤T98G细胞的增殖、黏附、迁移、侵袭能力。更多还原

【Abstract】 Objective To investigate the effects of anlotinib on the adhesion, migration, invasion and epithelial-mesenchymal transition（EMT） of human glioma cells. Methods Human glioma T98G cells were cultured in vitro and divided into control group（no intervention）, experimental group(2.5 μmol·L^-1 anlotinib group, 5 μmol·L^-1 anlotinib group, 10 μmol·L^-1 anlotinib group) and positive drug group(50 mg·L^-1 5-fluorouracil) for 24 hours.Cell proliferation, adhesion, migration, invasion and EMT-related protein expression were analyzed by cell count（CCK-8）, cell adhesion assay, scratch assay, Transwell and Western blotting（WB）. Results Compared with the control group, the proliferative activity of 5 μmol·L^-1, 10 μmol·L^-1 and positive drug groups was significantly decreased（P<0.05）, and the adhesion, migration and invasion ability of T98G cells in the experimental group and positive drug group were significantly decreased（P<0.05）. The expression levels of fibrin（FN）, Vimentin and N-cadherin were significantly down-regulated（P<0.05）, while the expression levels of E-cadherin were significantly up-regulated（P<0.05）. The higher the concentration, the more significant the change. Compared with positive drug group, the cell proliferation activity, adhesion, migration invasion ability, and the protein levels of N-cadherin, Vimentin and FN were up-regulated, while the protein level of E-cadherin was down-regulated in the 2.5 μmol·L^-1 and 5 μmol·L^-1 anlotinib groupsd（P<0.05）. There was no significant difference between the 10 μmol·L^-1 antirotinib group and the positive group（P>0.05）. Conclusion Anlotinib may inhibit the proliferation, adhesion, migration and invasion ability of human glioma T98G cells by inhibiting the process of EMT.更多还原