Effect of epigallocatechin-3-gallate on radiosensitivity of CNE-1 cells
10.3760/cma.j.issn.0254-5098.2012.03.004
- VernacularTitle:表没食子儿茶素没食子酸酯对人鼻咽癌CNE-1细胞辐射敏感性的影响
- Author:
Lin ZHAO
;
Kekang SUN
;
Linling SHEN
;
Yang JIAO
;
Jiaying XU
;
Saijun FAN
- Publication Type:Journal Article
- Keywords:
EGCG;
Nasopharyngeal carcinoma;
Radiosensitivity;
Cell cycle;
Apoptosis
- From:
Chinese Journal of Radiological Medicine and Protection
2012;32(3):236-240
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of EGCG on the radiosensitivity of human nasopharyngeal carcinoma CNE-1 cells.Methods CNE-1 cells were divided into four groups:control,EGCG treatment,UVC or X-ray exposure,and EGCG combined with UVC or X-rays.After treatment with different concentrations of EGCG for 24,48 and 72 h and UVC or X-rays,cell growth was determined with MTT assay,cell survival was measured with clonogenic assay,cell cycle was deteeted with flow cytometry,cell apoptosis was detected by the annexin V-FITC cell apoptosis kit,and protein expression was assayed by Westem blot.Results EGCG inhibited cell growth in a dose-and time-dependent manner(r =0.817and 0.364).Compared with UVC or X-ray irradiation alone,the radiosensitivity of CNE-1 cells was enhanced by 2 h pre-treatment of 50 μmol/L EGCG,which disrupted S phase arrest caused by UVC( t =18.68,P ＜ 0.05 ) and increased the population of S and G2/M arrest caused by X-rays ( t =7.11 and 6.99,P ＜0.05 ).UVC could cause a significant increase of sub-G1 population( t =6.67,P ＜ 0.05 ) and Annexin V-FITC assay indicated apoptosis was further elevated by EGCG ( t =10.28,P ＜ 0.05 ).However,no significant induction of apoptosis was observed in the cells either irradiated with X-rays alone or combinationly treated with EGCG and X-rays.The combination treatment of EGCG and UVC significantly increased the expression of Bax and Caspase-3 proteins,but failed to affect Bcl-2 protein expression.Conclusions EGCG enhances the growth inhibition of CNE-1 cells caused by UVC or X-rays,which is relevant to apoptosis induction or cell cycle arrest.
