Physalin A induces G2/M phase cell cycle arrest in human non-small cell lung cancer cells: involvement of the p38 MAPK/ROS pathway

被引:50
|
作者
Kang, Ning [1 ,2 ]
Jian, Jun-feng [5 ]
Cao, Shi-jie [4 ]
Zhang, Qiang [1 ]
Mao, Yi-wei [5 ]
Huang, Yi-yuan [1 ]
Peng, Yan-fei [1 ]
Qiu, Feng [3 ]
Gao, Xiu-mei [2 ]
机构
[1] Tianjin Univ Tradit Chinese Med, Sch Integrat Med, 312 Anshanxi Rd, Tianjin 300193, Peoples R China
[2] Tianjin Univ Tradit Chinese Med, Tianjin State Key Lab Modern Chinese Med, 312 Anshanxi Rd, Tianjin 300193, Peoples R China
[3] Tianjin Univ Tradit Chinese Med, Coll Tradit Chinese Med, 312 Anshanxi Rd, Tianjin 300193, Peoples R China
[4] Shenyang Pharmaceut Univ, Dept Nat Prod Chem, 103 Wenhua Rd, Shenyang 110016, Peoples R China
[5] Shenyang Pharmaceut Univ, Dept Biochem & Mol Biol, 103 Wenhua Rd, Shenyang 110016, Peoples R China
基金
中国国家自然科学基金; 中国博士后科学基金;
关键词
Physalin A; G2/M cell cycle arrest; p38; Reactive oxygen species (ROS); Non-small cell lung cancer (NSCLC); PROTEIN-KINASE PATHWAYS; HUMAN-MELANOMA CELLS; MAMMALIAN-CELLS; DNA-DAMAGE; IN-VITRO; APOPTOSIS; GROWTH; ACTIVATION; AUTOPHAGY; INHIBITOR;
D O I
10.1007/s11010-016-2686-1
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Physalin A (PA) is an active withanolide isolated from Physalis alkekengi var. franchetii, a traditional Chinese herbal medicine named Jindenglong, which has long been used for the treatment of sore throat, hepatitis, and tumors in China. In the present study, we firstly investigated the effects of PA on proliferation and cell cycle distribution of the human non-small cell lung cancer (NSCLC) A549 cell line, and the potential mechanisms involved. Here, PA inhibited cell growth in dose- and time-dependent manners. Treatment of A549 cells with 28.4 mu M PA for 24 h resulted in approximately 50 % cell death. PA increased the amount of intracellular ROS and the proportion of cells in G2/M. G2/M arrest was attenuated by the addition of ROS scavenger NAC. ERK and P38 were triggered by PA through phosphorylation in a time-dependent manner. The phosphorylation of ERK and P38 were not attenuated by the addition of NAC, but the use of the p38 inhibitor could reduce, at least in part, PA-induced ROS and the proportion of cells in G2/M. PA induces G2/M cell cycle arrest in A549 cells involving in the p38 MAPK/ROS pathway. This study suggests that PA might be a promising therapeutic agent against NSCLC.
引用
收藏
页码:145 / 155
页数:11
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