塞来昔布对人鼻咽癌CNE-2细胞生长抑制及放射增敏研究

目的 研究塞来昔布对人鼻咽癌细胞系CNE-2细胞生长影响及有无放射增敏作用.方法 (1)细胞生长抑制研究:用MTT法检测细胞生长抑制,流式细胞术检测细胞周期分布及凋亡,透射电子显微镜观察细胞凋亡形态,SP法检测细胞COX-2表达.(2)放射增敏研究:随机设置照射对照、药物对照、单纯照射、药物+照射组,其中成克隆实验单次照射2、4、6、8、10 Gy,细胞周期分布和凋亡实验单次照射6 Gy.结果 塞来昔布显著抑制CNE-2细胞生长并呈浓度和时间依赖性,IC50为80 μmol/L.细胞周期分布显示G0+G1期细胞显著升高(47.03±2.76:56.17±1.95,t=4.68,P=0.010),而S、G2+M期细胞明显下降(33.07±1.86:24.87±1.76,t=5.54,P=0.010;19.30±0.53:17.73±0.83.t=2.75,P=0.050)并呈浓度依赖性.凋亡率显著增高(1.57±0.47:10.47±0.31,t=27.39,P=0.000)并呈浓度依赖性.电镜观察到细胞皱缩、核质浓缩、核碎裂等凋亡形态学改变.SP法检测塞来昔布显著下调CNE-2中COX-2表达[17.48±0.34、12.82±0.51(t=13.20,P=0.00)].塞来昔布的放射增敏比(D0值比为1.74:1.52)为1.15.4个组别细胞周期分布结果 显示单纯照射、药物+照射组的G2+M期细胞明显高于照射对照、药物对照组(68.00±1.65、54.27±5.74、17.60±0.80、14.86±1.23,t=47.70,P=0.000;t=11.63,P=0.000),且单纯照射与药物+照射组间也不同(t=3.99,P=0.020);单纯照射、药物+照射组的细胞凋亡率也明显高于照射对照、药物对照组(4.83±0.97、9.50±1.35、1.33±0.36、2.28±0.42,t=4.67,P=0.01;t=8.81,P=0.000),且单纯照射与药物+照射组也不同(t=4.85,P=0.010).结论 塞来昔布能抑制人鼻咽癌CNE-2细胞生长和诱导凋亡,其机制可能涉及COX-2依赖途径.塞来昔布还能增强CNE-2细胞放射敏感性,可能机制与抑制放射后亚致死损伤修复、直接抑制细胞增殖和增强细胞对放射诱导凋亡率有关.     

塞来昔布对人鼻咽癌CNE-2细胞生长抑制及放射增敏研究

Objective To investigate the growth inhibition and radiosensitization of Celecoxib in hu-man nasopharyngeal carcinoma cell line CNE-2. Methods CNE-2 growth inhibition by Celecoxib was eval-uated by MTT method. Apoptosis-related changes in morphology were observed by transmission electron mi-croscopy (TEM). Cell cycle distribution and apoptosis rate were measured by flowcytometry (FCM). The ex-pression of COX-2 protein was observed by SP method after the treatment of Celecoxib. Cells were randomly planted into four groups: irradiation control(Ci), drug group(Cd), irradiation group(R), and Celecoxib plus irradiation group(D+R). Single irradiation of 2,4,6,8,and 10 Gy were administered for colonogenic assay. Cell cycle distribution and apoptosis rate were analyzed at 6 Gy irradiation. Results The growth of CNE-2 cell was inhibited by celecoxib in a dose-and time-dependent manner, the IC50 was 80 μmol/L After the treatment, cell ratio of GO and G, phases was increased (47.03±2.76 vs 56.17±1.95, t=4.68, P= 0.010), whereas the ratio of S and G2/M phases was decreased (33.07±1.86 vs 24.87±1.76, t=5.54, P = 0.010; 19.30±0.53: 17.73±0.83, t=2.75, P=0.050), and the apoptosis rate was increased (1.57±0.47:10.47±0.31, t = 27.39, P = 0.000) in a dose-dependent manner. Apoptosis with nuclear chromatin condensation, fragmentation and cell shrinkage was found by TEM. SP method showed that Celeib decreased COX-2 expression (17.48±0.34 vs 12.82±0.51,t=13.20,P =0.00). The sensitivity ratio(D0) was 1.15. FCM showed that the percentage of cells in G2/M phase was significanty more in R and D+R groups than in Ci and Cd groups (68.00±1.65,54.27±5.74,17.60±0.80,14.86±1.23, t=47.70,P=0.000; t=11.63, P=0.000), and also significantly different between R group and D + R group (t=3.99, P= 0.020). The apoptosis rate was higher in R and D + R groups than Ci and Cd groups(4.83±0.97,9.50± 1.35,1.33±0.86 and 2.28±0.42,t=4.67,P=0.010;t=8.81, P=0.000), D + R group than R group(t =4.85,P=0.010). Conclusions Celecoxib can markedly inhibit the growth and induce apoptosis in CNE-2 cells,which may depend on COX-2 pathway. Celeeoxib potently enhances the radiosensitivity of CNE-2 cells,which may due to the repair inhibit of radiation-induced DNA damage, inhibit of cell proliferation,and enhancement of cell apoptosis after irradiation.     

塞来昔布对人鼻咽癌CNE-2细胞生长抑制及放射增敏研究

Objective To investigate the growth inhibition and radiosensitization of Celecoxib in hu-man nasopharyngeal carcinoma cell line CNE-2. Methods CNE-2 growth inhibition by Celecoxib was eval-uated by MTT method. Apoptosis-related changes in morphology were observed by transmission electron mi-croscopy (TEM). Cell cycle distribution and apoptosis rate were measured by flowcytometry (FCM). The ex-pression of COX-2 protein was observed by SP method after the treatment of Celecoxib. Cells were randomly planted into four groups: irradiation control(Ci), drug group(Cd), irradiation group(R), and Celecoxib plus irradiation group(D+R). Single irradiation of 2,4,6,8,and 10 Gy were administered for colonogenic assay. Cell cycle distribution and apoptosis rate were analyzed at 6 Gy irradiation. Results The growth of CNE-2 cell was inhibited by celecoxib in a dose-and time-dependent manner, the IC50 was 80 μmol/L After the treatment, cell ratio of GO and G, phases was increased (47.03±2.76 vs 56.17±1.95, t=4.68, P= 0.010), whereas the ratio of S and G2/M phases was decreased (33.07±1.86 vs 24.87±1.76, t=5.54, P = 0.010; 19.30±0.53: 17.73±0.83, t=2.75, P=0.050), and the apoptosis rate was increased (1.57±0.47:10.47±0.31, t = 27.39, P = 0.000) in a dose-dependent manner. Apoptosis with nuclear chromatin condensation, fragmentation and cell shrinkage was found by TEM. SP method showed that Celeib decreased COX-2 expression (17.48±0.34 vs 12.82±0.51,t=13.20,P =0.00). The sensitivity ratio(D0) was 1.15. FCM showed that the percentage of cells in G2/M phase was significanty more in R and D+R groups than in Ci and Cd groups (68.00±1.65,54.27±5.74,17.60±0.80,14.86±1.23, t=47.70,P=0.000; t=11.63, P=0.000), and also significantly different between R group and D + R group (t=3.99, P= 0.020). The apoptosis rate was higher in R and D + R groups than Ci and Cd groups(4.83±0.97,9.50± 1.35,1.33±0.86 and 2.28±0.42,t=4.67,P=0.010;t=8.81, P=0.000), D + R group than R group(t =4.85,P=0.010). Conclusions Celecoxib can markedly inhibit the growth and induce apoptosis in CNE-2 cells,which may depend on COX-2 pathway. Celeeoxib potently enhances the radiosensitivity of CNE-2 cells,which may due to the repair inhibit of radiation-induced DNA damage, inhibit of cell proliferation,and enhancement of cell apoptosis after irradiation.     

塞来昔布对人鼻咽癌CNE-2细胞生长抑制及放射增敏研究

Objective To investigate the growth inhibition and radiosensitization of Celecoxib in hu-man nasopharyngeal carcinoma cell line CNE-2. Methods CNE-2 growth inhibition by Celecoxib was eval-uated by MTT method. Apoptosis-related changes in morphology were observed by transmission electron mi-croscopy (TEM). Cell cycle distribution and apoptosis rate were measured by flowcytometry (FCM). The ex-pression of COX-2 protein was observed by SP method after the treatment of Celecoxib. Cells were randomly planted into four groups: irradiation control(Ci), drug group(Cd), irradiation group(R), and Celecoxib plus irradiation group(D+R). Single irradiation of 2,4,6,8,and 10 Gy were administered for colonogenic assay. Cell cycle distribution and apoptosis rate were analyzed at 6 Gy irradiation. Results The growth of CNE-2 cell was inhibited by celecoxib in a dose-and time-dependent manner, the IC50 was 80 μmol/L After the treatment, cell ratio of GO and G, phases was increased (47.03±2.76 vs 56.17±1.95, t=4.68, P= 0.010), whereas the ratio of S and G2/M phases was decreased (33.07±1.86 vs 24.87±1.76, t=5.54, P = 0.010; 19.30±0.53: 17.73±0.83, t=2.75, P=0.050), and the apoptosis rate was increased (1.57±0.47:10.47±0.31, t = 27.39, P = 0.000) in a dose-dependent manner. Apoptosis with nuclear chromatin condensation, fragmentation and cell shrinkage was found by TEM. SP method showed that Celeib decreased COX-2 expression (17.48±0.34 vs 12.82±0.51,t=13.20,P =0.00). The sensitivity ratio(D0) was 1.15. FCM showed that the percentage of cells in G2/M phase was significanty more in R and D+R groups than in Ci and Cd groups (68.00±1.65,54.27±5.74,17.60±0.80,14.86±1.23, t=47.70,P=0.000; t=11.63, P=0.000), and also significantly different between R group and D + R group (t=3.99, P= 0.020). The apoptosis rate was higher in R and D + R groups than Ci and Cd groups(4.83±0.97,9.50± 1.35,1.33±0.86 and 2.28±0.42,t=4.67,P=0.010;t=8.81, P=0.000), D + R group than R group(t =4.85,P=0.010). Conclusions Celecoxib can markedly inhibit the growth and induce apoptosis in CNE-2 cells,which may depend on COX-2 pathway. Celeeoxib potently enhances the radiosensitivity of CNE-2 cells,which may due to the repair inhibit of radiation-induced DNA damage, inhibit of cell proliferation,and enhancement of cell apoptosis after irradiation.     

塞来昔布对人鼻咽癌CNE-2细胞生长抑制及放射增敏研究

Objective To investigate the growth inhibition and radiosensitization of Celecoxib in hu-man nasopharyngeal carcinoma cell line CNE-2. Methods CNE-2 growth inhibition by Celecoxib was eval-uated by MTT method. Apoptosis-related changes in morphology were observed by transmission electron mi-croscopy (TEM). Cell cycle distribution and apoptosis rate were measured by flowcytometry (FCM). The ex-pression of COX-2 protein was observed by SP method after the treatment of Celecoxib. Cells were randomly planted into four groups: irradiation control(Ci), drug group(Cd), irradiation group(R), and Celecoxib plus irradiation group(D+R). Single irradiation of 2,4,6,8,and 10 Gy were administered for colonogenic assay. Cell cycle distribution and apoptosis rate were analyzed at 6 Gy irradiation. Results The growth of CNE-2 cell was inhibited by celecoxib in a dose-and time-dependent manner, the IC50 was 80 μmol/L After the treatment, cell ratio of GO and G, phases was increased (47.03±2.76 vs 56.17±1.95, t=4.68, P= 0.010), whereas the ratio of S and G2/M phases was decreased (33.07±1.86 vs 24.87±1.76, t=5.54, P = 0.010; 19.30±0.53: 17.73±0.83, t=2.75, P=0.050), and the apoptosis rate was increased (1.57±0.47:10.47±0.31, t = 27.39, P = 0.000) in a dose-dependent manner. Apoptosis with nuclear chromatin condensation, fragmentation and cell shrinkage was found by TEM. SP method showed that Celeib decreased COX-2 expression (17.48±0.34 vs 12.82±0.51,t=13.20,P =0.00). The sensitivity ratio(D0) was 1.15. FCM showed that the percentage of cells in G2/M phase was significanty more in R and D+R groups than in Ci and Cd groups (68.00±1.65,54.27±5.74,17.60±0.80,14.86±1.23, t=47.70,P=0.000; t=11.63, P=0.000), and also significantly different between R group and D + R group (t=3.99, P= 0.020). The apoptosis rate was higher in R and D + R groups than Ci and Cd groups(4.83±0.97,9.50± 1.35,1.33±0.86 and 2.28±0.42,t=4.67,P=0.010;t=8.81, P=0.000), D + R group than R group(t =4.85,P=0.010). Conclusions Celecoxib can markedly inhibit the growth and induce apoptosis in CNE-2 cells,which may depend on COX-2 pathway. Celeeoxib potently enhances the radiosensitivity of CNE-2 cells,which may due to the repair inhibit of radiation-induced DNA damage, inhibit of cell proliferation,and enhancement of cell apoptosis after irradiation.     

塞来昔布对人鼻咽癌CNE-2细胞生长抑制及放射增敏研究

Objective To investigate the growth inhibition and radiosensitization of Celecoxib in hu-man nasopharyngeal carcinoma cell line CNE-2. Methods CNE-2 growth inhibition by Celecoxib was eval-uated by MTT method. Apoptosis-related changes in morphology were observed by transmission electron mi-croscopy (TEM). Cell cycle distribution and apoptosis rate were measured by flowcytometry (FCM). The ex-pression of COX-2 protein was observed by SP method after the treatment of Celecoxib. Cells were randomly planted into four groups: irradiation control(Ci), drug group(Cd), irradiation group(R), and Celecoxib plus irradiation group(D+R). Single irradiation of 2,4,6,8,and 10 Gy were administered for colonogenic assay. Cell cycle distribution and apoptosis rate were analyzed at 6 Gy irradiation. Results The growth of CNE-2 cell was inhibited by celecoxib in a dose-and time-dependent manner, the IC50 was 80 μmol/L After the treatment, cell ratio of GO and G, phases was increased (47.03±2.76 vs 56.17±1.95, t=4.68, P= 0.010), whereas the ratio of S and G2/M phases was decreased (33.07±1.86 vs 24.87±1.76, t=5.54, P = 0.010; 19.30±0.53: 17.73±0.83, t=2.75, P=0.050), and the apoptosis rate was increased (1.57±0.47:10.47±0.31, t = 27.39, P = 0.000) in a dose-dependent manner. Apoptosis with nuclear chromatin condensation, fragmentation and cell shrinkage was found by TEM. SP method showed that Celeib decreased COX-2 expression (17.48±0.34 vs 12.82±0.51,t=13.20,P =0.00). The sensitivity ratio(D0) was 1.15. FCM showed that the percentage of cells in G2/M phase was significanty more in R and D+R groups than in Ci and Cd groups (68.00±1.65,54.27±5.74,17.60±0.80,14.86±1.23, t=47.70,P=0.000; t=11.63, P=0.000), and also significantly different between R group and D + R group (t=3.99, P= 0.020). The apoptosis rate was higher in R and D + R groups than Ci and Cd groups(4.83±0.97,9.50± 1.35,1.33±0.86 and 2.28±0.42,t=4.67,P=0.010;t=8.81, P=0.000), D + R group than R group(t =4.85,P=0.010). Conclusions Celecoxib can markedly inhibit the growth and induce apoptosis in CNE-2 cells,which may depend on COX-2 pathway. Celeeoxib potently enhances the radiosensitivity of CNE-2 cells,which may due to the repair inhibit of radiation-induced DNA damage, inhibit of cell proliferation,and enhancement of cell apoptosis after irradiation.     

塞来昔布对人鼻咽癌CNE-2细胞生长抑制及放射增敏研究

Objective To investigate the growth inhibition and radiosensitization of Celecoxib in hu-man nasopharyngeal carcinoma cell line CNE-2. Methods CNE-2 growth inhibition by Celecoxib was eval-uated by MTT method. Apoptosis-related changes in morphology were observed by transmission electron mi-croscopy (TEM). Cell cycle distribution and apoptosis rate were measured by flowcytometry (FCM). The ex-pression of COX-2 protein was observed by SP method after the treatment of Celecoxib. Cells were randomly planted into four groups: irradiation control(Ci), drug group(Cd), irradiation group(R), and Celecoxib plus irradiation group(D+R). Single irradiation of 2,4,6,8,and 10 Gy were administered for colonogenic assay. Cell cycle distribution and apoptosis rate were analyzed at 6 Gy irradiation. Results The growth of CNE-2 cell was inhibited by celecoxib in a dose-and time-dependent manner, the IC50 was 80 μmol/L After the treatment, cell ratio of GO and G, phases was increased (47.03±2.76 vs 56.17±1.95, t=4.68, P= 0.010), whereas the ratio of S and G2/M phases was decreased (33.07±1.86 vs 24.87±1.76, t=5.54, P = 0.010; 19.30±0.53: 17.73±0.83, t=2.75, P=0.050), and the apoptosis rate was increased (1.57±0.47:10.47±0.31, t = 27.39, P = 0.000) in a dose-dependent manner. Apoptosis with nuclear chromatin condensation, fragmentation and cell shrinkage was found by TEM. SP method showed that Celeib decreased COX-2 expression (17.48±0.34 vs 12.82±0.51,t=13.20,P =0.00). The sensitivity ratio(D0) was 1.15. FCM showed that the percentage of cells in G2/M phase was significanty more in R and D+R groups than in Ci and Cd groups (68.00±1.65,54.27±5.74,17.60±0.80,14.86±1.23, t=47.70,P=0.000; t=11.63, P=0.000), and also significantly different between R group and D + R group (t=3.99, P= 0.020). The apoptosis rate was higher in R and D + R groups than Ci and Cd groups(4.83±0.97,9.50± 1.35,1.33±0.86 and 2.28±0.42,t=4.67,P=0.010;t=8.81, P=0.000), D + R group than R group(t =4.85,P=0.010). Conclusions Celecoxib can markedly inhibit the growth and induce apoptosis in CNE-2 cells,which may depend on COX-2 pathway. Celeeoxib potently enhances the radiosensitivity of CNE-2 cells,which may due to the repair inhibit of radiation-induced DNA damage, inhibit of cell proliferation,and enhancement of cell apoptosis after irradiation.     

塞来昔布对人鼻咽癌CNE-2细胞生长抑制及放射增敏研究

Objective To investigate the growth inhibition and radiosensitization of Celecoxib in hu-man nasopharyngeal carcinoma cell line CNE-2. Methods CNE-2 growth inhibition by Celecoxib was eval-uated by MTT method. Apoptosis-related changes in morphology were observed by transmission electron mi-croscopy (TEM). Cell cycle distribution and apoptosis rate were measured by flowcytometry (FCM). The ex-pression of COX-2 protein was observed by SP method after the treatment of Celecoxib. Cells were randomly planted into four groups: irradiation control(Ci), drug group(Cd), irradiation group(R), and Celecoxib plus irradiation group(D+R). Single irradiation of 2,4,6,8,and 10 Gy were administered for colonogenic assay. Cell cycle distribution and apoptosis rate were analyzed at 6 Gy irradiation. Results The growth of CNE-2 cell was inhibited by celecoxib in a dose-and time-dependent manner, the IC50 was 80 μmol/L After the treatment, cell ratio of GO and G, phases was increased (47.03±2.76 vs 56.17±1.95, t=4.68, P= 0.010), whereas the ratio of S and G2/M phases was decreased (33.07±1.86 vs 24.87±1.76, t=5.54, P = 0.010; 19.30±0.53: 17.73±0.83, t=2.75, P=0.050), and the apoptosis rate was increased (1.57±0.47:10.47±0.31, t = 27.39, P = 0.000) in a dose-dependent manner. Apoptosis with nuclear chromatin condensation, fragmentation and cell shrinkage was found by TEM. SP method showed that Celeib decreased COX-2 expression (17.48±0.34 vs 12.82±0.51,t=13.20,P =0.00). The sensitivity ratio(D0) was 1.15. FCM showed that the percentage of cells in G2/M phase was significanty more in R and D+R groups than in Ci and Cd groups (68.00±1.65,54.27±5.74,17.60±0.80,14.86±1.23, t=47.70,P=0.000; t=11.63, P=0.000), and also significantly different between R group and D + R group (t=3.99, P= 0.020). The apoptosis rate was higher in R and D + R groups than Ci and Cd groups(4.83±0.97,9.50± 1.35,1.33±0.86 and 2.28±0.42,t=4.67,P=0.010;t=8.81, P=0.000), D + R group than R group(t =4.85,P=0.010). Conclusions Celecoxib can markedly inhibit the growth and induce apoptosis in CNE-2 cells,which may depend on COX-2 pathway. Celeeoxib potently enhances the radiosensitivity of CNE-2 cells,which may due to the repair inhibit of radiation-induced DNA damage, inhibit of cell proliferation,and enhancement of cell apoptosis after irradiation.     

塞来昔布对人鼻咽癌CNE-2细胞生长抑制及放射增敏研究

Objective To investigate the growth inhibition and radiosensitization of Celecoxib in hu-man nasopharyngeal carcinoma cell line CNE-2. Methods CNE-2 growth inhibition by Celecoxib was eval-uated by MTT method. Apoptosis-related changes in morphology were observed by transmission electron mi-croscopy (TEM). Cell cycle distribution and apoptosis rate were measured by flowcytometry (FCM). The ex-pression of COX-2 protein was observed by SP method after the treatment of Celecoxib. Cells were randomly planted into four groups: irradiation control(Ci), drug group(Cd), irradiation group(R), and Celecoxib plus irradiation group(D+R). Single irradiation of 2,4,6,8,and 10 Gy were administered for colonogenic assay. Cell cycle distribution and apoptosis rate were analyzed at 6 Gy irradiation. Results The growth of CNE-2 cell was inhibited by celecoxib in a dose-and time-dependent manner, the IC50 was 80 μmol/L After the treatment, cell ratio of GO and G, phases was increased (47.03±2.76 vs 56.17±1.95, t=4.68, P= 0.010), whereas the ratio of S and G2/M phases was decreased (33.07±1.86 vs 24.87±1.76, t=5.54, P = 0.010; 19.30±0.53: 17.73±0.83, t=2.75, P=0.050), and the apoptosis rate was increased (1.57±0.47:10.47±0.31, t = 27.39, P = 0.000) in a dose-dependent manner. Apoptosis with nuclear chromatin condensation, fragmentation and cell shrinkage was found by TEM. SP method showed that Celeib decreased COX-2 expression (17.48±0.34 vs 12.82±0.51,t=13.20,P =0.00). The sensitivity ratio(D0) was 1.15. FCM showed that the percentage of cells in G2/M phase was significanty more in R and D+R groups than in Ci and Cd groups (68.00±1.65,54.27±5.74,17.60±0.80,14.86±1.23, t=47.70,P=0.000; t=11.63, P=0.000), and also significantly different between R group and D + R group (t=3.99, P= 0.020). The apoptosis rate was higher in R and D + R groups than Ci and Cd groups(4.83±0.97,9.50± 1.35,1.33±0.86 and 2.28±0.42,t=4.67,P=0.010;t=8.81, P=0.000), D + R group than R group(t =4.85,P=0.010). Conclusions Celecoxib can markedly inhibit the growth and induce apoptosis in CNE-2 cells,which may depend on COX-2 pathway. Celeeoxib potently enhances the radiosensitivity of CNE-2 cells,which may due to the repair inhibit of radiation-induced DNA damage, inhibit of cell proliferation,and enhancement of cell apoptosis after irradiation.     

塞来昔布对人鼻咽癌CNE-2细胞生长抑制及放射增敏研究

Objective To investigate the growth inhibition and radiosensitization of Celecoxib in hu-man nasopharyngeal carcinoma cell line CNE-2. Methods CNE-2 growth inhibition by Celecoxib was eval-uated by MTT method. Apoptosis-related changes in morphology were observed by transmission electron mi-croscopy (TEM). Cell cycle distribution and apoptosis rate were measured by flowcytometry (FCM). The ex-pression of COX-2 protein was observed by SP method after the treatment of Celecoxib. Cells were randomly planted into four groups: irradiation control(Ci), drug group(Cd), irradiation group(R), and Celecoxib plus irradiation group(D+R). Single irradiation of 2,4,6,8,and 10 Gy were administered for colonogenic assay. Cell cycle distribution and apoptosis rate were analyzed at 6 Gy irradiation. Results The growth of CNE-2 cell was inhibited by celecoxib in a dose-and time-dependent manner, the IC50 was 80 μmol/L After the treatment, cell ratio of GO and G, phases was increased (47.03±2.76 vs 56.17±1.95, t=4.68, P= 0.010), whereas the ratio of S and G2/M phases was decreased (33.07±1.86 vs 24.87±1.76, t=5.54, P = 0.010; 19.30±0.53: 17.73±0.83, t=2.75, P=0.050), and the apoptosis rate was increased (1.57±0.47:10.47±0.31, t = 27.39, P = 0.000) in a dose-dependent manner. Apoptosis with nuclear chromatin condensation, fragmentation and cell shrinkage was found by TEM. SP method showed that Celeib decreased COX-2 expression (17.48±0.34 vs 12.82±0.51,t=13.20,P =0.00). The sensitivity ratio(D0) was 1.15. FCM showed that the percentage of cells in G2/M phase was significanty more in R and D+R groups than in Ci and Cd groups (68.00±1.65,54.27±5.74,17.60±0.80,14.86±1.23, t=47.70,P=0.000; t=11.63, P=0.000), and also significantly different between R group and D + R group (t=3.99, P= 0.020). The apoptosis rate was higher in R and D + R groups than Ci and Cd groups(4.83±0.97,9.50± 1.35,1.33±0.86 and 2.28±0.42,t=4.67,P=0.010;t=8.81, P=0.000), D + R group than R group(t =4.85,P=0.010). Conclusions Celecoxib can markedly inhibit the growth and induce apoptosis in CNE-2 cells,which may depend on COX-2 pathway. Celeeoxib potently enhances the radiosensitivity of CNE-2 cells,which may due to the repair inhibit of radiation-induced DNA damage, inhibit of cell proliferation,and enhancement of cell apoptosis after irradiation.