Effects of celecoxib on the proliferation and apoptosis of human nasopharyngeal carcinoma cell line CNE-2.
- Author:
Xinhua XU
1
;
Fang YI
;
Xiangyang FU
;
Daojun LI
;
Qiao HUANG
;
Jingtao DU
Author Information
1. Department of Oncology, Central Hospital of Yichang City, the First Clinical Medical College of Three Gorges University, Yichang, 443003, China. xuxinhua@medmail.com.cn
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Celecoxib;
Cell Line, Tumor;
Cell Proliferation;
drug effects;
Cyclooxygenase 2 Inhibitors;
pharmacology;
Humans;
Nasopharyngeal Neoplasms;
pathology;
Pyrazoles;
pharmacology;
Sulfonamides;
pharmacology
- From:
Journal of Clinical Otorhinolaryngology Head and Neck Surgery
2009;23(15):682-685
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To detect the effect of Celecoxib on the proliferation and apoptosis of human nasopharyngeal carcinoma cell line CNE-2.
METHOD:The growth inhibition rate of CNE-2 by Celecoxib was evaluated with MTT method. Apoptosis related morphology changes were observed with transmission electron microscopy (TEM). The cell cycle and apoptosis were measured with flow cytometric method (FCM). Apoptotic index (AI) was counted by the TDT-mediated dUTP-biotin nick end-labeling (TUNEL) assay.
RESULT:The growth of CNE-2 cell was inhibited by celecoxib in a dose-and time-dependent manner. Apoptosis with nuclear chromatin condensation, cell shrinkage, periplasm loss and the formation of apoptotic bodies was observed with TEM. Apoptotic rates of CNE-2 cells treated with 80 and 100 micromol/L celecoxib were (10.47+/-0.18)% and (20.17+/-0.55)% respectively, significantly higher than those of the control group (1.57+/-0.27)% with FCM. The percentage of G0/G1 phase cells increased, whereas the S and G2/M phases cells decreased in a dose-dependent manner after the treatment. TUNEL assay showed that the apoptosis ratio (AI) of CNE-2 treated with Celecoxib was higher than control group (P<0.01).
CONCLUSION:Celecoxib can inhibit the growth of human nasopharyngeal carcinoma cell line CNE-2 and induce the cell apoptosis, which may be related to blocking the cell cycle progress of CNE-2 cells.