虎杖甙对人乳腺细胞系MDA-MB-231增殖、侵袭和迁移的调节作用

Effects of polydatin on cell proliferation,migration and invasion of breast cell line MDA-MB-231

目的:探究虎杖甙(Polydatin)对人乳腺癌细胞MDA-MB-231细胞增殖、侵袭和迁移的作用。方法:将乳腺癌细胞MDA-MB-231分为MDA-MB-231组、Polydatin(0.2μmol/L)组、Polydatin(0.5μmol/L)组和Polydatin(1μmol/L)组,并分别用0、0.2、0.5和1μmol/L的虎杖甙处理MDA-MB-231细胞,CCK8检测细胞增殖倍数,Transwell实验检测MDA-MB-231细胞的侵袭能力,划痕实验检测MDA-MB-231细胞的迁移能力,免疫印迹检测细胞增殖及侵袭相关蛋白Ki67、血管内皮生长因子(VEGF)和基质金属蛋白酶(MMP-9)的表达。结果:与MDA-MB-231组比较,Polydatin(0.2μmol/L)组、Polydatin(0.5μmol/L)组和Polydatin(1μmol/L)组细胞增殖倍数显著降低,Ki67蛋白表达水平也显著降低,侵袭细胞数量明显减少,划痕闭合率与MDA-MB-231组比较也显著降低;VEGF和MMP-9的蛋白表达水平与MDA-MB-231组比较也显著降低。结论:虎杖甙能抑制乳腺癌MDA-MB-231细胞增殖、侵袭和迁移。

Objective: To investigate the effects of polydatin on proliferation,migration and invasion of breast cancer cell line MDA-MB-231. Methods: Cells were divided into MDA-MB-231,Polydatin(0.2 μmol/L),Polydatin(0.5 μmol/L) and Polydatin (1 μmol/L) groups,and cells were treated with different concentration of polydatin(0,0.2,0.5,1 μmol/L).CCK8 assay was performed for cell growth fold,the invasion ability of MDA-MB-231 cells was determined by Transwell assay,the migration ability was measured by wound healing assay,and the expression of proliferation-,migration- and invasion-related proteins,including Ki67,vascular endothelial growth factor(VEGF)and matrix metalloproteinase-9(MMP-9)were measured by Western blot. Results: Compared with MDA-MB-231 group,the growth folds of cells in Polydatin(0.2 μmol/L),Polydatin(0.5 μmol/L) and Polydatin(1 μmol/L) groups was decreased significantly,and the level of Ki67 down-regulated notably.Meanwhile,compared with MDA-MB-231 group,the numbers of invasive cells in Polydatin(0.2 μmol/L),Polydatin(0.5 μmol/L)and Polydatin(1 μmol/L)group were decreased,and wound closure rates were decreased makedly.In addition,the protein levels of VEGF and MMP-9 in Polydatin(0.2 μmol/L),Polydatin (0.5 μmol/L) and Polydatin(1 μmol/L) group were down-regulated significantly compared with MDA-MB-231 group. Conclusion: Polydatin can inhibit proliferation,invasion and migration of MDA-MB-231 cell.