详细信息

Total saponins of Bolbostemma paniculatum (maxim.) Franquet exert antitumor activity against MDA-MB-231 human breast cancer cells via inhibiting PI3K/Akt/mTOR pathway  ( SCI-EXPANDED收录)   被引量:13

文献类型:期刊文献

英文题名:Total saponins of Bolbostemma paniculatum (maxim.) Franquet exert antitumor activity against MDA-MB-231 human breast cancer cells via inhibiting PI3K/Akt/mTOR pathway

作者:Dou, Jian-Wei[1,2];Shang, Rong-Guo[1,2];Lei, Xiao-Qin[3,4];Li, Kang-Le[1,2];Guo, Zhan-Zi[5];Ye, Kai[5];Yang, Xiao-Juan[5];Li, Yu-Wei[3,4];Zhou, Yun-Yun[3,4];Yao, Jia[6];Huang, Qian[6]

第一作者:Dou, Jian-Wei

通信作者:Huang, Q[1]

机构:[1]Xi An Jiao Tong Univ, Sch Pharm, Xian 710061, Shaanxi, Peoples R China;[2]Shaanxi Key Lab Qiyao Resources & Antitumor Act, Xian 710061, Shaanxi, Peoples R China;[3]Xi An Jiao Tong Univ, Affiliated Guangren Hosp, Dept Ophthalmol, Xian 710004, Shaanxi, Peoples R China;[4]Xian 4 Hosp, Dept Ophthalmol, Xian 710004, Shaanxi, Peoples R China;[5]Gansu Univ Chinese Med, Sch Basic Med, Lanzhou 730000, Gansu, Peoples R China;[6]Shaanxi Univ Chinese Med, Xian Hosp Tradit Chinese Med, Xian 710021, Shaanxi, Peoples R China

第一机构:Xi An Jiao Tong Univ, Sch Pharm, Xian 710061, Shaanxi, Peoples R China

通信机构:[1]corresponding author), Shaanxi Univ Chinese Med, Xian Hosp Tradit Chinese Med, Xian 710021, Shaanxi, Peoples R China.

年份:2019

卷号:19

期号:1

外文期刊名:BMC COMPLEMENTARY AND ALTERNATIVE MEDICINE

收录:;WOS:【SCI-EXPANDED(收录号:WOS:000495595700002)】;

基金:The present study was was supported by grants from The National Natural Science Foundation of China (grant nos. 81573983, 81873311 and 81674028) and Health Commission of Xi'an city Subject (grant no. SZJ201907).

语种:英文

外文关键词:Bolbostemma paniculatum (maxim) Franquet; Total saponins; MDA-MB-231 cells; PI3K; Akt; mTOR; signaling pathway

摘要:Background The aim of the present study was to examine the effects of the Bolbostemma paniculatum (Maxim.) Franquet (BP) active compound, BP total saponins (BPTS), on MDA-MB-231 cells, and investigate the underlying mechanism regarding BPTS-mediated attenuation of the PI3K/Akt/mTOR pathway. Methods The effect of BPTS on cytotoxicity, induction of apoptosis and migration on MDA-MB-231 cells at three different concentrations was investigated. A CCK-8 assay, wound-healing assay and flow cytometry were used to demonstrate the effects of BPTS. Additionally, expression of the primary members of the PI3K/Akt/mTOR signaling pathway was assessed using western blotting. To verify the underlying mechanisms, a PI3K inhibitor and an mTOR inhibitor were used. Results BPTS inhibited proliferation of MDA-MB-231 cells with an IC50 value of 10 mu g/mL at 48 h. BPTS inhibited migration of MDA-MB-231 cells, and the western blot results demonstrated that BPTS reduced p-PI3K, p-Akt and p-mTOR protein expression levels in MDA-MB-231 cells. Additionally, the results were confirmed using a PI3K inhibitor and an mTOR inhibitor. BPTS decreased proliferation and migration of MDA-MB-231 cells possibly through inhibiting the PI3K/Akt/mTOR signaling pathway. Conclusions The results highlight the therapeutic potential of BPTS for treating patients with triple-negative breast cancer.

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