中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2014年
5期
1042-1044
,共3页
杨洋%樊玉霞%刘东雷%吴恺%温丰标%赵松
楊洋%樊玉霞%劉東雷%吳愷%溫豐標%趙鬆
양양%번옥하%류동뢰%오개%온봉표%조송
蛋白酶体抑制剂%顺铂%脱噬作用%食管鳞癌
蛋白酶體抑製劑%順鉑%脫噬作用%食管鱗癌
단백매체억제제%순박%탈서작용%식관린암
Proteosome inhibitor%Cisplatin%Apoptosis%Esophageal squamous cell carcinoma
目的 探讨蛋白酶体抑制剂MG132联合顺铂对食管鳞癌细胞的杀伤作用及其机制.方法 分别以顺铂(100 mg/L)、MG132(5μmol/L)及顺铂+MG132处理食管鳞癌EC9706细胞24h,细胞计数试剂盒(CCK-8)法检测细胞活力,膜联蛋白V(Annexin V)-异硫氰酸荧光素(FITC)细胞凋亡检测试剂盒定量检测细胞凋亡率,Westem blot检测凋亡相关蛋白半胱氨酰天冬氨酸特异性蛋白酶(Caspase)-8、Caspase-3和核转录因子(NF)-κB的表达.结果 MG132可以抑制肿瘤细胞的增殖,增强顺铂对食管鳞癌细胞的杀伤作用,使细胞存活率从(68.19±3.41)%降低至(29.37±4.16)%(P<0.05).MG132联合顺铂处理组的细胞凋亡率为(68.45±2.58)%,明显高于单独处理组的(23.55±1.23)%和(25.87±2.07)%(P<0.01).联合用药组细胞Caspase-8、Caspase-3的表达水平高于顺铂处理组,但NF-κB较单独顺铂处理组明显下降(P<0.05).结论 MG132通过抑制肿瘤细胞增殖,促进凋亡,提高顺铂对食管鳞癌细胞的杀伤作用.
目的 探討蛋白酶體抑製劑MG132聯閤順鉑對食管鱗癌細胞的殺傷作用及其機製.方法 分彆以順鉑(100 mg/L)、MG132(5μmol/L)及順鉑+MG132處理食管鱗癌EC9706細胞24h,細胞計數試劑盒(CCK-8)法檢測細胞活力,膜聯蛋白V(Annexin V)-異硫氰痠熒光素(FITC)細胞凋亡檢測試劑盒定量檢測細胞凋亡率,Westem blot檢測凋亡相關蛋白半胱氨酰天鼕氨痠特異性蛋白酶(Caspase)-8、Caspase-3和覈轉錄因子(NF)-κB的錶達.結果 MG132可以抑製腫瘤細胞的增殖,增彊順鉑對食管鱗癌細胞的殺傷作用,使細胞存活率從(68.19±3.41)%降低至(29.37±4.16)%(P<0.05).MG132聯閤順鉑處理組的細胞凋亡率為(68.45±2.58)%,明顯高于單獨處理組的(23.55±1.23)%和(25.87±2.07)%(P<0.01).聯閤用藥組細胞Caspase-8、Caspase-3的錶達水平高于順鉑處理組,但NF-κB較單獨順鉑處理組明顯下降(P<0.05).結論 MG132通過抑製腫瘤細胞增殖,促進凋亡,提高順鉑對食管鱗癌細胞的殺傷作用.
목적 탐토단백매체억제제MG132연합순박대식관린암세포적살상작용급기궤제.방법 분별이순박(100 mg/L)、MG132(5μmol/L)급순박+MG132처리식관린암EC9706세포24h,세포계수시제합(CCK-8)법검측세포활력,막련단백V(Annexin V)-이류청산형광소(FITC)세포조망검측시제합정량검측세포조망솔,Westem blot검측조망상관단백반광안선천동안산특이성단백매(Caspase)-8、Caspase-3화핵전록인자(NF)-κB적표체.결과 MG132가이억제종류세포적증식,증강순박대식관린암세포적살상작용,사세포존활솔종(68.19±3.41)%강저지(29.37±4.16)%(P<0.05).MG132연합순박처리조적세포조망솔위(68.45±2.58)%,명현고우단독처리조적(23.55±1.23)%화(25.87±2.07)%(P<0.01).연합용약조세포Caspase-8、Caspase-3적표체수평고우순박처리조,단NF-κB교단독순박처리조명현하강(P<0.05).결론 MG132통과억제종류세포증식,촉진조망,제고순박대식관린암세포적살상작용.
Objective To investigate the antitumor activity of proteasome inhibitor MG132 in human esophageal squamous cancer cells.Methods EC9706 cells were treated with 100 mg/L cisplatin,5 pmol/L MG132 and cisplatin + MG132 for 24 h.Cell viability was measured by using cell counting kit-8(CCK-8) assay.The percentages of apoptotic cells were analyzed by using Annexin V-fluoresceine isothio-cyanate (FITC) apoptosis detection kit.Western blotting assay was used to detect the expression of nuclear factor-κB (NF-κB),Caspase-8 and-3.Results Exposure of cells to cisplatin combined with MG132 re-suited in a marked increase in the cell cytotoxicity of EC9706 cells as compared with the single agent.The combined cisplatin and MG132 treatment induced more apoptosis in tumor cells than in cisplatin treatmentalone (68.45 ±2.58 vs.23.5 ± 1.23% ;P <0.01).MG132 significantly enhanced cisplatin-induced ap-optosis in association with the activation of Caspase-3 and-8.These events were accompanied by the down-regulation of NF-κB.Conclusion These findings demonstrate a novel mechanism by which proteasome inhibitor MG132 potentiates cisplatin-induced apoptosis in human esophageal squamous cell carcinoma.