5-FU诱导白血病细胞凋亡的分子机制研究  

Molecular mechenism of apoptosis of leukamic cells induced by 5-FU

作　　者：祝瑾[1] 贾筱琴[2] 程宏[1] 

机构地区：[1]扬州大学医学院生化室,江苏扬州225001 [2]扬州大学医学院病理室,江苏扬州225001

出　　处：《中华肿瘤防治杂志》2006年第8期586-588,共3页Chinese Journal of Cancer Prevention and Treatment

基　　金：扬州大学自然科学基金(PK0410191)

摘　　要：目的:检测化疗药物5氟尿嘧啶(5FU)引起的T淋巴白血病细胞凋亡,及与之相关蛋白的表达和信号通路,为探索T淋巴细胞凋亡分子机制打下基础,为相关肿瘤的治疗提供依据。方法:用5FU(10μg/mL)刺激Jurkat细胞36h以诱导细胞发生凋亡,用流式细胞术和MTS比色法检测细胞存活率,计算细胞凋亡率;用Western blot检测p53的表达和caspase3的变化;向Jurkat细胞中瞬时共转染野生型或突变型pCMV p53和pEGFP c1检测p53在5FU诱导的T淋巴细胞凋亡中的作用。结果:5FU能诱导Jurkat细胞凋亡并伴随p53表达增加及caspase3的活化;野生型p53过表达可明显增加细胞对5FU的敏感性。结论:5FU诱导的T淋巴白血病细胞凋亡的分子机制可能涉及p53及caspase3。OBJECTIVE： To investigate the signal pathway and expression of related proteins in apoptosis of T lymphocyte （leukemia） induced by 5-fluorouracil （5-FU）, providing a novel insight and information in the apoptosis signaling pathways induced by 5-FU and an important implication for the clinical therapy of T-lymphocyte leukemia. METHODS： Jurkat cells treated with 5-FU （10 μg/mL） for 36 h were used to detect the viability with MTS assay and to detect caspase-3 and p53 expression with Western blot. To investigate the role of p53 in 5-FU-induced cell death of T lymphocyte, wild type or mutant pCMV-p53 were cotransfected transiently with pEGFP-cl into Jurkat cells. RESULTS： 5-FU induced apoptosis of Jurkat cells with activation of caspase-3. Cells transfected with wild-type p53 exhibited more sensitivity to 5-FU than cells transfected with mutant p53. CONCLUSION： Molecular mechanism of apoptosis of T-lymphocyte leukemia induced by 5-FU may involve caspase-3 and p53. p53 expression plays an important role in apoptosis induced by 5-FU.

关 键 词：白血病 蛋白质P53 细胞凋亡 氟尿嘧啶 免疫印迹法 流式细胞术 

分 类 号：R733.7[医药卫生—肿瘤]