摘要
目的:探究阿昔替尼(axitinib)对人肾上腺皮质癌SW-13细胞生物学行为的影响。方法:CCK-8法检测不同浓度axitinib对SW-13细胞活力的影响;流式细胞术检测细胞周期分布;Annexin V/PI双染法检测细胞凋亡率;划痕愈合实验及Transwell侵袭实验观察细胞迁移及侵袭的情况;Western blot实验检测细胞中血管内皮生长因子受体2(VEGFR2)、细胞外信号调节蛋白激酶1/2(ERK1/2)和p-ERK1/2的蛋白水平。结果:Axitinib能抑制SW-13细胞活力,阻滞细胞于G_2/M期,促进细胞凋亡,并抑制SW-13细胞的迁移及侵袭能力(P<0.05);axitinib可以下调SW-13细胞VEGFR2和p-ERK1/2的蛋白水平(P<0.05)。结论:Axitinib可以抑制SW-13细胞生长、阻滞细胞周期、促进细胞凋亡并抑制其迁移和侵袭,其作用机制可能与抑制VEGFR2的表达和减少ERK1/2的磷酸化有关。
AIM:To investigate the effects of axitinib on the biological behavior of adrenocortical carcinoma cell line SW-13.METHODS:CCK-8 assay was used to measured the viability of SW-13 cells treated with axitinib at different concentrations.The cell cycle distribution was analyzed by flow cytometry.The apoptotic rate was also analyzed by flow cytometry with Annexin V/PI double staining.Wound healing experiment and Transwell invasion assay were used to observe cell migration and invasion abilities,respectively.The protein levels of vascular endothelial growth factor receptor 2(VEGFR2),extracellular regulated protein kinases 1/2(ERK1/2)and p-ERK1/2 were determined by Western blot.RESULTS:After treated with axitinib,the viability of SW-13 cells was significantly inhibited,the cell cycle was blocked in G 2/M phase,and the apoptosis rate was increased.The migration and invasion abilities of SW-13 cells were markedly inhibited by axitinib(P<0.01).The protein levels of VEGFR2 and p-ERK1/2 in the SW-13 cells were significantly decreased with axitinib treatment(P<0.01).CONCLUSION:Axitinib inhibits the viability,blocks the cell cycle,promotes cell apoptosis,and inhibits the migration and invasion abilities of SW-13 cells.The mechanism may be related to inhibition of VEGFR2 expression and reduction of ERK1/2 phosphorylation.
作者
杨涛玮
汪帮琦
胡卫列
YANG Tao-wei;WANG Bang-qi;HU Wei-lie(Southern Medical University,Guangzhou 510515,China;Department of Urology,General Hospital of Southern Theater Command,PLA,Guangzhou 510010.China)
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2019年第5期819-824,共6页
Chinese Journal of Pathophysiology
基金
广东省医学科研基金项目(No.A2017442)