Effects of Costunolide on Cell Cycle Distribution and Apoptosis of Breast Cancer SK-BR- 3 Cells
- VernacularTitle:木香烃内酯对乳腺癌SK-BR-3细胞周期分布及凋亡的影响
- Author:
Qiang MA
1
,
2
;
Jie CHEN
1
;
Jiawei MIAO
1
;
Shu XIONG
1
;
Yi PANG
1
,
2
;
Xuesong DENG
1
Author Information
1. Dept. of Basic Medicine，Chongqing Three Gorges Medical College，Chongqing 404120，China
2. Chongqing Key Laboratory of Development and Utilization of Genuine Medicinal Materials in Three Gorges Reservoir Area，Chongqing 404120，China
- Publication Type:Journal Article
- Keywords:
Costunolide;
SK-BR-3 cells;
Cell proliferation;
Cell cycle;
Cell apoptosis
- From:
China Pharmacy
2021;32(17):2073-2078
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE：To study the effects of costunolide （COS）on the cell cycle distribution and apoptosis of human breast cancer SK-BR- 3 cells and its mechanism. METHODS ：Human breast cancer SK-BR- 3 cells were divided into blank control group，and COS groups of 10，20，30，40，50 μmol/L. MTT assay was used to detect the effects of COS on cell proliferation. SK-BR-3 cells were divided into blank control group ，COS low ，medium and high concentration groups （10，20，30 μmol/L）. After cultured for 24 h，flow cytometry was used to detect the distribution of cell cycle. Hoechst 33258 fluorescence staining was used to detect cell apoptosis. Western blot assay was used to detect the expression of p 53，caspase-3，Bcl-2，Bax，p21，CDK2 and cyclinE. RESULTS ：Compared with blank control group ，COS could significantly inhibit the proliferation of SK-BR- 3 cells（P＜ 0.05 or P＜0.01），and in a dose and time-dependent manner. Low ，medium and high concentrations of COS could induce cell apoptosis and arrest cell at G 1/S phase （P＜0.05 or P＜0.01），could significantly up-regulate the protein expression of p 53， caspase-3，Bax and p 21（P＜0.05 or P＜0.01），and could significantly down-regulate the protein expression of Bcl- 2，CDK2 and cyclinE（P＜0.01）. CONCLUSIONS ：COS can inhibit the proliferation of human breast cancer SK-BR- 3 cells and induce cell apoptosis and cell cycle arrest. The mechanism may be related to the regulation of p 53/Bax/Bcl-2/caspase-3 apoptosis signal pathway.
