Inhibitory effects of Gubenyiliu Formula Ⅱ(固本抑瘤Ⅱ 号) and its blood activation prescriptions on the growth of MCF-7human breast cancer xengrafts in nude mice
Objective: The present study aimed to investigate the inhibitory effects of Gubenyiliu Formula II (GFII) and its blood activation prescriptions on the growth of MCF-7 human breast cancer xengrafts in nude mice,and explore their mechanisms of action.Methods: After the establishment of the MCF-7 human breast cancer xenograft model in nude mice,the mice in the GFII and its blood activation groups were administered with GFII (6.56 g/ml) and blood activation prescriptions (1.65 g/ml) by gavage for 28 days,respectively.The tumor volume and weight were measured twice a week throughout the treatment period.Apoptotic cells were identified by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling.The expression of microtubule associated protein 1 light chain 3 (LC3) was examined by immunohistochemistry,and western blotting analysis was performed to detect the expression of anti-apoptotic protein Bcl-2 andLC3 Meanwhile,the effects on PI3K/Akt/mTOR signaling pathway were also determined by western blotting analysis.Results: Compared with the control group,GFII group and its blood activation prescriptions could significantly inhibit the growth of MCF-7 human breast cancer xenografts in nude mice.The expression of Bcl-2 protein was lower in the GFII and blood activation groups than in the control group,whereas both the percentage of apoptotic cells and LC3-II/LC3-I ratio were higher than in the control group.In addition,a significantly reduced expression of phospho-Akt,phospho-mTOR and mTOR was observed in the blood activation group (P<0.05).Conclusions: To some extent,GFII and its blood activation prescriptions can exert their inhibitory effect on the growth of MCF-7 human breast cancer xenografts by inducing the cell apoptosis and autophagy.In addition to the induction of cell apoptosis,we also found that the blood activation prescriptions of GFII could induce cell autophagy by inhibiting of PI3K/AKT/mTOR signaling pathway,and then suppress the breast cancer cell growth.
breast cancer apoptosis autophagy PI3K/Akt/mTOR Gubenyiliu formula Ⅱ
马丛 王笑民 于明薇 张甘霖 南楠 张怡 曹可心 李晋萍
国内会议
第五届国际中医、中西医结合肿瘤学术交流大会暨第十四届全国中西医结合肿瘤学术大会
广州
中文
1-15
2014-07-01（万方平台首次上网日期，不代表论文的发表时间）