Effect of evodiamine on the proliferation and apoptosis of A549 human lung cancer cells

被引:49
|
作者
Lin, Li [1 ]
Ren, Li [2 ]
Wen, Liujing [3 ]
Wang, Yu [4 ]
Qi, Jin [5 ]
机构
[1] Tianjin Med Univ Canc Inst & Hosp, Dept Thorac Oncol, Natl Clin Res Ctr Canc, Lung Canc Diag & Treatment Ctr,Key Lab Canc Preve, Tianjin 300060, Peoples R China
[2] Tianjin Med Univ Canc Inst & Hosp, Dept Clin Lab, Natl Clin Res Ctr Canc, Key Lab Canc Prevent & Therapy,Tianjins Clin Res, Tianjin 300060, Peoples R China
[3] Tianjin Med Univ Canc Inst & Hosp, Dept Pharm, Natl Clin Res Ctr Canc, Key Lab Canc Prevent & Therapy,Tianjins Clin Res, Tianjin 300060, Peoples R China
[4] Tianjin Univ Tradit Chinese Med, Dept Radiol, Tianjin State Key Lab Modern Chinese Med, Tianjin 300193, Peoples R China
[5] Tianjin Med Univ Canc Inst & Hosp, Dept Radiol, Natl Clin Res Ctr Canc, Key Lab Canc Prevent & Therapy,Tianjins Clin Res, Tianjin 300060, Peoples R China
关键词
evodiamine; lung cancer; apoptosis; oxidative damage; SONIC HEDGEHOG; ADENOCARCINOMA CELLS; QUINOLONE ALKALOIDS; MEDIATED APOPTOSIS; IN-VITRO; EXPRESSION; PROMOTES; PATHWAY; DYSFUNCTION; INHIBITION;
D O I
10.3892/mmr.2016.5575
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Evodia rutaecarpa is a plant, which has antitumor activity. Evodiamine is an alkaloid with antitumor activity present in E. rutaecarpa and has potential to be developed into a therapeutic antitumor agent. The present study investigated the effect of evodiamine on the proliferation of A549 human lung cancer cells and the mechanism underlying these effects. The results indicated that evodiamine significantly inhibited proliferation, induced apoptosis and the expression of reactive oxygen species, arrested the cell cycle, regulated the expression of Survivin, Bcl-2 and Cyclin B1, regulated the activity of caspase-3/8 and glutathione in tumor cells, and decreased the activity of AKT/nuclear factor-B (NF-B) and Sonic hedgehog/GLI family zinc finger 1 (SHH/GLI1) signaling pathways in A549 cells. In conclusion, the evodiamine-induced inhibition of the proliferation of A549 lung cancer cells may be attributable to its ability to promote oxidative injury in the cells, induce apoptosis, arrest the cell cycle and regulate the AKT/NF-B and SHH/GLI1 signaling pathways, subsequently controlling the expression of tumor-associated genes.
引用
收藏
页码:2832 / 2838
页数:7
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