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. Key words: EGCG; Nasopharyngeal carcinoma; Radiosensitivity; Cell cycle; Apoptosis

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.