OBJECTIVE： To investigate the effects of ophiopogonin D on human breast cancer MCF-7 cells METHODS： Cell viability was assessed by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide and colony formation ...OBJECTIVE： To investigate the effects of ophiopogonin D on human breast cancer MCF-7 cells METHODS： Cell viability was assessed by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide and colony formation experiments. Cell cycle was measured with cell cycle flow cytometry and a living cell assay. Apoptosis and terminal deoxynucleoitidyl transferase-mediated dUTP nick end labeling assays were performed to detect the apoptosis of MCF-7 cells induced by ophiopogonin D. Finally, Western blotting was used to explore the mechanism. RESULTS： Exposure of cells to ophiopogonin D resulted in marked decreases in viable cells and colony formation with a dose-dependent manner. Treatment of these cells with ophiopogonin D also resulted in cell cycle arrest at the G2/M phase, and increased apoptosis. Mechanistically, ophiopogonin D-induced G2/M cell cycle arrest was associated with down-regulation of cyclin BI. Furthermore, activation of caspase-8 and caspase-9 was involved in ophiopogonin D-induced apoptosis. CONCLUSION： The data suggested that ophiopogonin D inhibits MCF-7 cell growth via the induction of cell cycle arrest at the G2/M phase.展开更多
基金Financial assistance was provided by grants from the National Natural Science Foundation of China(No.81173141)
文摘OBJECTIVE： To investigate the effects of ophiopogonin D on human breast cancer MCF-7 cells METHODS： Cell viability was assessed by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide and colony formation experiments. Cell cycle was measured with cell cycle flow cytometry and a living cell assay. Apoptosis and terminal deoxynucleoitidyl transferase-mediated dUTP nick end labeling assays were performed to detect the apoptosis of MCF-7 cells induced by ophiopogonin D. Finally, Western blotting was used to explore the mechanism. RESULTS： Exposure of cells to ophiopogonin D resulted in marked decreases in viable cells and colony formation with a dose-dependent manner. Treatment of these cells with ophiopogonin D also resulted in cell cycle arrest at the G2/M phase, and increased apoptosis. Mechanistically, ophiopogonin D-induced G2/M cell cycle arrest was associated with down-regulation of cyclin BI. Furthermore, activation of caspase-8 and caspase-9 was involved in ophiopogonin D-induced apoptosis. CONCLUSION： The data suggested that ophiopogonin D inhibits MCF-7 cell growth via the induction of cell cycle arrest at the G2/M phase.
