中华耳鼻咽喉头颈外科杂志
中華耳鼻嚥喉頭頸外科雜誌
중화이비인후두경외과잡지
CHINESE JOURNAL OF OTORHINOLARYNGOLOGY HEAD AND NECK SURGERY
2011年
10期
854-858
,共5页
李仕晟%唐青来%王树辉%陈月红%刘家佳%王爽%杨新明
李仕晟%唐青來%王樹輝%陳月紅%劉傢佳%王爽%楊新明
리사성%당청래%왕수휘%진월홍%류가가%왕상%양신명
TNF相关凋亡诱导配体%色酮类%吗啉类%1-磷脂酰肌醇3-激酶%细胞凋亡%鼻咽肿瘤
TNF相關凋亡誘導配體%色酮類%嗎啉類%1-燐脂酰肌醇3-激酶%細胞凋亡%鼻嚥腫瘤
TNF상관조망유도배체%색동류%마람류%1-린지선기순3-격매%세포조망%비인종류
TNF-related apoptosis-inducing ligand%Chromones%Morpholines%1-Phosphatidylinositol 3-kinase%Apoptosis%Nasopharyngeal neoplasms
目的 观察联合肿瘤坏死因子相关凋亡诱导配体(tumor necrosis factor related apoptosis-inducing ligand,TRAIL)和阻断PI3-K-Akt信号通路,对鼻咽癌细胞株CNE-2的影响,并探索其可能的机制.方法 用TRAIL和PI3-K特异性抑制剂LY294002单独和联合处理鼻咽癌细胞株CNE-2,采用四甲基偶氮唑蓝法检测细胞存活率,流式细胞仪进行细胞凋亡率的分析,Western blot检测相关蛋白表达及Caspase活化程度.用TRAIL和LY294002单独和联合处理人良性成纤维细胞株MRC-5,检测细胞存活率.结果 TRAIL质量浓度＞1 ng/ml时,联合处理组CNE-2细胞存活率大于TRAIL单独处理组存活率(P值均＜0.05)；当TRAIL质量浓度为10 ng/ml和100 ng/ml,联合处理组细胞凋亡率明显大于TRAIL单独处理组细胞凋亡率(t值为7.167和7.206,P值均＜0.05)；与TRAIL单独处理组相比,联合处理组出现明显的Caspase-8、Caspase-3、Caspase-9活化增多.两组对比Akt、p-Akt、Bcl-2表达无明显改变；在MRC-5中,对照组、TRAIL单独处理组和联合处理组细胞存活率差异无统计学意义(P＞0.05).结论 联合TRAIL和阻断PI3-K-Akt信号通路对抑制鼻咽癌细胞株CNE-2生长,诱导细胞凋亡具有协同作用,其可能机制是诱导线粒体依赖途径.
目的 觀察聯閤腫瘤壞死因子相關凋亡誘導配體(tumor necrosis factor related apoptosis-inducing ligand,TRAIL)和阻斷PI3-K-Akt信號通路,對鼻嚥癌細胞株CNE-2的影響,併探索其可能的機製.方法 用TRAIL和PI3-K特異性抑製劑LY294002單獨和聯閤處理鼻嚥癌細胞株CNE-2,採用四甲基偶氮唑藍法檢測細胞存活率,流式細胞儀進行細胞凋亡率的分析,Western blot檢測相關蛋白錶達及Caspase活化程度.用TRAIL和LY294002單獨和聯閤處理人良性成纖維細胞株MRC-5,檢測細胞存活率.結果 TRAIL質量濃度＞1 ng/ml時,聯閤處理組CNE-2細胞存活率大于TRAIL單獨處理組存活率(P值均＜0.05)；噹TRAIL質量濃度為10 ng/ml和100 ng/ml,聯閤處理組細胞凋亡率明顯大于TRAIL單獨處理組細胞凋亡率(t值為7.167和7.206,P值均＜0.05)；與TRAIL單獨處理組相比,聯閤處理組齣現明顯的Caspase-8、Caspase-3、Caspase-9活化增多.兩組對比Akt、p-Akt、Bcl-2錶達無明顯改變；在MRC-5中,對照組、TRAIL單獨處理組和聯閤處理組細胞存活率差異無統計學意義(P＞0.05).結論 聯閤TRAIL和阻斷PI3-K-Akt信號通路對抑製鼻嚥癌細胞株CNE-2生長,誘導細胞凋亡具有協同作用,其可能機製是誘導線粒體依賴途徑.
목적 관찰연합종류배사인자상관조망유도배체(tumor necrosis factor related apoptosis-inducing ligand,TRAIL)화조단PI3-K-Akt신호통로,대비인암세포주CNE-2적영향,병탐색기가능적궤제.방법 용TRAIL화PI3-K특이성억제제LY294002단독화연합처리비인암세포주CNE-2,채용사갑기우담서람법검측세포존활솔,류식세포의진행세포조망솔적분석,Western blot검측상관단백표체급Caspase활화정도.용TRAIL화LY294002단독화연합처리인량성성섬유세포주MRC-5,검측세포존활솔.결과 TRAIL질량농도＞1 ng/ml시,연합처리조CNE-2세포존활솔대우TRAIL단독처리조존활솔(P치균＜0.05)；당TRAIL질량농도위10 ng/ml화100 ng/ml,연합처리조세포조망솔명현대우TRAIL단독처리조세포조망솔(t치위7.167화7.206,P치균＜0.05)；여TRAIL단독처리조상비,연합처리조출현명현적Caspase-8、Caspase-3、Caspase-9활화증다.량조대비Akt、p-Akt、Bcl-2표체무명현개변；재MRC-5중,대조조、TRAIL단독처리조화연합처리조세포존활솔차이무통계학의의(P＞0.05).결론 연합TRAIL화조단PI3-K-Akt신호통로대억제비인암세포주CNE-2생장,유도세포조망구유협동작용,기가능궤제시유도선립체의뢰도경.
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.
