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肿瘤坏死因子相关凋亡诱导配体联合PI3-K-Akt抑制对鼻咽癌细胞的影响

[Effects of combining tumor necrosis factor related apoptosis-inducing ligand with PI3-K-Akt inhibition on nasopharyngeal carcinoma cell].

作者信息

Li Shi-sheng, Tang Qing-lai, Wang Shu-hui, Chen Yue-hong, Liu Jia-jia, Wang Shuang, Yang Xin-ming

机构信息

Department of Otorhinolaryngology Head and Neck Surgery, the Second Xiangya Hospital Central South University, Changsha 410011, China.

出版信息

Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2011 Oct;46(10):854-8.

Abstract

OBJECTIVE

To study the effects of combinative therapy of tumor necrosis factor related apoptosis-inducing ligand (TRAIL) and PI3-K-Akt inhibitor on the growth and apoptosis of nasopharyngeal carcinoma (NPC) cells and underlying mechanisms.

METHODS

With cell growth assay, flow cytometric analysis and Western blotting, the effects of TRAIL and PI3-K-Akt special inhibitor (LY294002) on cell growth, apoptosis and related proteins expressions in CNE-2 cell lines were studied.

RESULTS

When concentrate of TRAIL>1 ng/ml, viability rate of cells in combinative treatment group with TRAIL and LY294002 was higher than that in the single treatment group with TRAIL (all P<0.05). When concentrate of TRAIL were 10 ng/ml and 100 ng/ml, the combinative treatment induced CNE-2 apoptosis more obviously than single treatments (t were 7.167 and 7.206, all P<0.05). The combination group showed more cleavage of Caspase-8, Caspase-3, Caspase-9 than single treatment groups.

CONCLUSIONS

Combinative application of TRAIL and PI3-K-Akt pathway inhibitor inhibits the growth of CNE-2 and induces apoptosis. The mitochondrial dependent pathway is implicated for the underlying mechanism.

摘要

目的

研究肿瘤坏死因子相关凋亡诱导配体(TRAIL)与PI3-K-Akt抑制剂联合治疗对鼻咽癌(NPC)细胞生长和凋亡的影响及其潜在机制。

方法

采用细胞生长实验、流式细胞术分析及蛋白质免疫印迹法,研究TRAIL和PI3-K-Akt特异性抑制剂(LY294002)对CNE-2细胞系细胞生长、凋亡及相关蛋白表达的影响。

结果

当TRAIL浓度>1 ng/ml时,TRAIL与LY294002联合治疗组细胞存活率高于TRAIL单药治疗组(均P<0.05)。当TRAIL浓度为10 ng/ml和100 ng/ml时,联合治疗比单药治疗更明显地诱导CNE-2细胞凋亡(t分别为7.167和7.206,均P<0.05)。联合治疗组比单药治疗组显示出更多的Caspase-8、Caspase-3、Caspase-9裂解。

结论

TRAIL与PI3-K-Akt通路抑制剂联合应用可抑制CNE-2细胞生长并诱导凋亡。线粒体依赖途径可能是其潜在机制。

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