Treatment Center of Oncology, The Fourth Affiliated Hospital of Harbin Medical University, NanGang, Harbin 150001, PR China.
Mol Med Rep. 2011 Nov-Dec;4(6):1313-9. doi: 10.3892/mmr.2011.574. Epub 2011 Aug 25.
The root of Polygonum multiflorum Thunb. (PM) is utilized to treat many diseases associated with aging. Research also indicates that PM inhibits the proliferation of certain types of cancer cells. The aim of the present study was to evaluate the inhibitory effect of PM extract (PME) on the proliferation of MCF-7 cells and to investigate the underlying mechanisms. Inhibition of the proliferation of MCF-7 cells was determined by the MTT assay. Cell cycle distribution and apoptotic rates were evaluated by flow cytometry, and cell cycle and apoptosis-related protein expression was assessed by Western blotting. Apoptotic characteristics of MCF-7 cells were detected by transmission electron microscopy. The present study showed that PME at doses of 100, 150, 200 and 250 µg/ml significantly inhibited proliferation of MCF-7 cells in a time- and dose-dependent manner. Flow cytometry showed that the cell apoptotic rates were 9.1 ± 1.67 and 17.7 ± 2.93% after treatment with 100 and 200 µg/ml PME for 48 h, respectively. The proportions of cells in the G2/M phase were 37.9 ± 1.47 and 42.0 ± 1.71% after treatment with 100 and 200 µg/ml PME for 24 h, respectively. Western blot analysis showed that PME down-regulated the protein expression of Cdc25B and Cdc25C phosphatases accompanied by an increase in phospho-Cdk1, and PME promoted cytochrome c release from mitochondria into the cytosol to activate caspase-9. The present study demonstrated that PME inhibited MCF-7 cell proliferation by inducing cell cycle arrest in the G2/M phase and promoting cell apoptosis. The effects of PME on MCF-7 cells were associated with the modulation of the expression levels of proteins involved in the cell cycle and apoptosis. These data suggest that PME has promise as a treatment against breast cancer by inhibiting the proliferation of cancer cells.
何首乌的根部被用于治疗许多与衰老相关的疾病。研究还表明,何首乌能抑制某些类型癌细胞的增殖。本研究旨在评估何首乌提取物(PME)对 MCF-7 细胞增殖的抑制作用,并探讨其潜在机制。采用 MTT 法测定 MCF-7 细胞增殖抑制率。采用流式细胞术检测细胞周期分布和凋亡率,Western blot 检测细胞周期和凋亡相关蛋白表达。透射电镜观察 MCF-7 细胞的凋亡特征。结果表明,PME 在 100、150、200 和 250μg/ml 剂量下,呈时间和剂量依赖性显著抑制 MCF-7 细胞增殖。流式细胞术显示,100 和 200μg/ml PME 作用 48 h 后细胞凋亡率分别为 9.1±1.67%和 17.7±2.93%。作用 24 h 后,细胞 G2/M 期比例分别为 37.9±1.47%和 42.0±1.71%。Western blot 分析显示,PME 下调 Cdc25B 和 Cdc25C 磷酸酶蛋白表达,同时磷酸化 Cdk1 增加,PME 促进细胞色素 c 从线粒体释放到细胞质中,激活 caspase-9。本研究表明,PME 通过诱导细胞周期 G2/M 期阻滞和促进细胞凋亡抑制 MCF-7 细胞增殖。PME 对 MCF-7 细胞的作用与调节细胞周期和凋亡相关蛋白的表达水平有关。这些数据表明,PME 通过抑制癌细胞增殖,有望成为治疗乳腺癌的一种方法。