Mechanisms and proliferation inhibitory effects of atractylenolide Ⅰ on SK-OV-3 and OVCAR-3 ovarian cancer cell
10.11659/jjssx.10E016046
- VernacularTitle:白术内酯Ⅰ抑制卵巢癌SK-OV-3与OVCAR-3细胞增殖作用机制的研究
- Author:
Fangyi LONG
;
Ping JIA
;
Huafei WANG
;
Yi QING
;
Mengjie HE
;
Xiaoli WANG
- Keywords:
atractylenolide Ⅰ;
proliferation;
cell cycle;
PI3K/AKT;
ovarian cancer
- From:
Journal of Regional Anatomy and Operative Surgery
2017;26(2):89-93
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the mechanisms and proliferation inhibitory effects of atractylenolide Ⅰ on SK-OV-3 and OVCAR-3 ovarian cancer cell.Methods SK-OV-3 and OVCAR-3 cells were treated with atractylenolide I with various concentrations at 24 hours,48 hours and 72 hours,and the changes in proliferation were detected by MTT assay.The cell cycles were measured by PI staining and flow cytometry,and the expressions of cyclin D1 and CDK1 were detected by ELISA assay.Western blot was then applied to investigate the effects of atractylenolide Ⅰ on PI3K/AKT signaling pathway in SK-OV-3 and OVCAR-3 cells.Results Atractylenolide I could significantly inhibit the proliferation of SK-OV-3 and OVCAR-3 cells,and its inhibitory effects were concentration and time dependent.In addition,atractylenolide I could also significantly reduce the proportion of cells in S phase and increase the proportion of cells in G2/M phase,and these effects were associated with the down-regulation of CDK1.The results of Western blot indicated that PI3K/AKT signaling pathway was involved in the inhibitory effects of atractylenolide Ⅰ on proliferation and cell cycle.Conclusion Atractylenolide I can down-regulate the expression of CDK1 in ovarian cancer SK-OV-3 and OVCAR-3 cells through PI3K/AKT pathway,which led to cell cycle arrest in G2/M phase,and played an important role in proliferation inhibition of tumor cells.
