Ellagic acid promotes A549 cell apoptosis via regulating the phosphoinositide 3-kinase/protein kinase B pathway

被引:35
作者
Liu, Qiong [1 ]
Liang, Xiaobing [1 ]
Niu, Chengwei [1 ]
Wang, Xuelan [1 ]
机构
[1] Sun Yat Sen Univ, Xinhua Coll, Med Expt Ctr, 19 Longdong Huamei Rd, Guangzhou 510520, Guangdong, Peoples R China
关键词
non-small cell lung cancer; A549; cells; apoptosis; phosphoinositide 3-kinase/protein kinase B; SIGNALING PATHWAY; CANCER; AKT; PROLIFERATION; INHIBITION; ACTIVATION;
D O I
10.3892/etm.2018.6193
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
The present study aimed to evaluate the anti-cancer effect of ellagic acid in human non-small cell lung cancer (NSCLC) A549 cells and to reveal the potential underlying mechanism. The effects of ellagic acid on the cell proliferation of A549 cells were determined by MTT assay. Cell cycle and apoptosis were measured with flow cytometry and Annexin V-propidium iodide staining. Western blotting was used to measure the expression levels of the phosphatidylinositol 3-kinase (PI3K)/protein kinas B (Akt) signaling pathway and apoptosis-associated proteins. It was demonstrated that ellagic acid exerted an inhibitory effect in the proliferation of human NSCLC A549 cells. Flow cytometry demonstrated that G1 phase retention and apoptosis rates were significantly increased after treatment with ellagic acid. Further investigation revealed that ellagic acid treatment diminished the phosphorylation of PI3K and Akt and regulated the expression of apoptosis-associated proteins in A549 cells. In conclusion, the present results indicated that ellagic acid suppresses cell proliferation, arrests cell cycle and induces apoptosis in human NSCLC A549 cells by inhibiting the PI3K/Akt signaling pathway.
引用
收藏
页码:347 / 352
页数:6
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