Inhibitory effect of 17-AAG combined with paclitaxel on proliferation of esophageal squa-mous cell carcinoma Eca-109 cells in vitro
- VernacularTitle:17-AAG联合紫杉醇对Eca-109食管癌细胞增殖的抑制作用
- Author:
Size CHEN
1
;
Xuemei CHEN
;
Yuqi LI
;
Shu YANG
;
Xianyi MO
;
Fan ZHANG
;
Kailan MO
;
Ying DING
Author Information
1. 广东药学院附属第一医院肿瘤科
- Keywords:
esophageal cancer;
17-AAG;
paclitaxel;
proliferation;
apoptosis
- From:
Journal of Southern Medical University
2015;(6):844-847
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of 17-AAG combined with paclitaxel (PTX) on the proliferation and apoptosis of esophageal squamous cell carcinoma cell line Eca-109 in vitro. Methods Eca-109 cells were treated with 17-AAG and PTX either alone or in combination. The proliferation of Eca-109 cells was detected by MTT assay, and the cell cycle changes and cell apoptosis were determined by flow cytometry. Results Compared with the control group, both 17-AAG and PTX significantly inhibited the proliferation of Eca-109 cells. A combined treatment of the cells with 0.5μmol/L PTX and 0.625μmol/L 17-AAG produced an obviously stronger inhibitory effect on the cell proliferation than either of the agents used alone (P<0.01). Flow cytometry showed that, 17-AAG and PTX used alone caused Eca-109 cell cycle arrest in G2/M phase and S phase, respectively, and their combined use caused cell cycle arrest in both G2/M and S phases. The cell apoptosis rates of Eca-109 cells treated with 17-AAG, PTX and their combination were 4.52%, 10.91%, and 29.88%, respectively, all significantly higher than that in the control group (1.32%); the combined treatment resulted in a distinct apoptotic peak that was significantly higher than that caused by either of the agents alone. Conclusion 17-AAG and PTX can inhibit cell proliferation and promote apoptosis of Eca-109 cells, and their combination produces stronger effects in inhibiting cell proliferation and increasing cell apoptosis.
