AMPK的激活调节COX-2对HT-29细胞增殖和凋亡的影响  

Effect of AMPK Activation via COX-2 Expression on HT-29 Cell Proliferation and Apoptosis

作　　者：陈琦[1] 邹岚[1] 梁后杰[1] 

机构地区：[1]第三军医大学西南医院肿瘤科,重庆市400038

出　　处：《中国肿瘤临床》2009年第14期823-826,共4页Chinese Journal of Clinical Oncology

基　　金：国家自然科学基金资助(编号:30873015)~~

摘　　要：目的:研究AMPK的激活在结肠癌HT-29细胞中对COX-2表达的影响,并探讨其对细胞增殖和凋亡的作用。方法:用Western Blot方法检测AMPK的激活对COX-2表达的影响,MTT法检测不同浓度、时间的AMPK激活剂AICAR和选择性COX-2抑制剂塞来昔布作用下的细胞存活率,流式细胞术检测细胞凋亡率,用MTT法检测二者联合对细胞增殖的影响。结果:AMPK被激活后COX-2蛋白表达减少,随着AICAR和塞来昔布作用浓度、时间增加,细胞存活率呈剂量和时间依赖性下降,塞来昔布组和AICAR组凋亡细胞增多,早期凋亡细胞及晚期凋亡细胞比例均高于对照组(P<0.05),AICAR和塞来昔布联用后细胞的存活率为(23.0±0.82)%,均低于AICAR组(54.0±2.86)%和塞来昔布组(57.0±2.54)%。结论:AMPK激活可以抑制COX-2表达对人结肠癌HT-29细胞产生增殖抑制和凋亡诱导效应,AICAR和塞来昔布二者联用具有协同作用。Objective： To investigate effect of AMPK activation on COX-2 expression, cell proliferation and apoptosis in colon cancer cell line HT-29. Methods： Western blot was used to study the influence of AMPK activation on COX-2 expression. Cell survival rate of HT-29 cells which were treated with AICAR and celecoxib in different dose and time was measured by MTT assay. Cell apoptosis rate was detected by FCM assay. Results： COX-2 expression in HT-29 cells was decreased when AMPK was activated. AICAR and celecoxib both inhibited the cell proliferation in a dose- and time-dependent manner. The cell apoptosis rate both in AICAR group and celecoxib group was much higher than that in the control group （P〈0.05）. Cell survival rate was （23.0 ± 0.82）% when celecoxib was combined with AICAR, lower than that in AICAR group and celecoxib group （P〈0.05）. Conclusion： AMPK activation could inhibit cell proliferation and induce cell apoptosis through regulating COX-2 expression. There is a synergistic effect when celecoxib is combined with AICAR.

关 键 词：AMPK AICAR COX-2 塞来昔布 结肠癌 

分 类 号：R735.35[医药卫生—肿瘤] R733.71[医药卫生—临床医学]