Licochalcone A inhibits PI3K/Akt/mTOR signaling pathway activation and promotes autophagy in breast cancer cells

被引：56

作者：

Xue, Lei ^{[1
]}

Zhang, Wei-Jie ^{[1
]}

Fan, Qing-Xia ^{[1
]}

Wang, Liu-Xing ^{[1
]}

机构：

[1] Zhengzhou Univ, Affiliated Hosp 1, Dept Oncol, 1 Jianshe East Rd, Zhengzhou 450052, Henan, Peoples R China

来源：

ONCOLOGY LETTERS | 2018年 / 15卷 / 02期

关键词：

Licochalcone A; breast cancer; autophagy; phosphoinositide 3-kinase/RAC-alpha serine-threonine-protein kinase/mammalian target of rapamycin; CARCINOMA CELLS; PROSTATE-CANCER; DOWN-REGULATION; IN-VITRO; APOPTOSIS; INVASION; INACTIVATION; GROWTH; AGENT;

D O I：

10.3892/ol.2017.7451

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Previous studies have demonstrated that Licochalcone A possesses anti-inflammatory, anticancer, anti-bacterial, anti-malarial and anti-parasitic activities. In the present study the potential anticancer effects of Licochalcone A on MCF-7 cells were investigated. Licochalcone A significantly decreased cell viability and promoted autophagy and apoptosis, as demonstrated by an MTT assay, acridine orange staining and Annexin V-fluorescein isothiocyanate staining, respectively. Western blot analyses demonstrated that Licochalcone A treatment activated the LC3-II signaling pathway while suppressing the phosphoinositide 3-kinase (PI3K)/RAC-alpha seri ne-threonine-protein kinase (A kt)/mammalian target of rapamycin (mTOR) signaling pathway. In addition, Licochalcone A significantly increased caspase-3 activity and significantly decreased B-cell lymphoma-2 expression. The results from the present study indicate that Licochalcone A inhibits PI3K/Akt/mTOR activation, and promotes autophagy and apoptosis in MCF-7 cells.

引用

页码：1869 / 1873

页数：5

共 23 条

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