Ophiopogonin D inhibits cell proliferation, causes cell cycle arrest at G2/M, and induces apoptosis in human breast carcinoma MCF-7 cells

• Published in: Journal of integrative medicine Vol. 14; no. 1; pp. 51 - 59
• Main Authors: Zang, Qing-qing, Zhang, Lu, Gao, Ning, Huang, Cheng
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 2016
• Subjects: antineoplastic agents, phytogenic; apoptosis; Apoptosis - drug effects; breast neoplasms; caspases; Cell Proliferation - drug effects; cyclin B1; G2 Phase Cell Cycle Checkpoints - drug effects; G2/M arrest; Humans; in vitro; M Phase Cell Cycle Checkpoints - drug effects; MCF-7 Cells; ophiopogonin D; Saponins - pharmacology; Spirostans - pharmacology; 乳腺癌; 皂苷; 细胞凋亡; 细胞周期阻滞; 细胞增殖; 麦冬; antineoplastic agents, phytogenic; G2/M arrest; breast neoplasms; in vitro; cyclin B1; apoptosis; caspases; ophiopogonin D
• ISSN: 2095-4964
• DOI: 10.1016/S2095-4964(16)60238-8

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.