5-Fu诱导结肠癌细胞凋亡与NF-κB活化及uPA表达的关系

 摘要] 目的 研究5-氟尿嘧啶（5-Fu）诱导结肠癌细胞HCT116凋亡与核转录因子-κB (NF-κB) 活化以及uPA表达的关系，并观察吡咯烷二硫氨基甲酸盐（PDTC）抑制NF-κB活化对5-Fu诱导结肠癌细胞凋亡及uPA表达的影响。方法 采用流式细胞仪Annexin Ⅴ-FITC法检测结肠癌细胞HCT116凋亡;采用免疫组织化学方法半定量分析HCT116细胞NF-κB及uPA表达的动态变化。结果 5-Fu在诱导HCT116细胞凋亡的同时有NF-κB活化，1umol/LPDTC能显著增加5-Fu诱导HCT116细胞凋亡及抑制5-Fu诱导的HCT116细胞NF-κB活化作用(P<0.05), uPA变化与NF-κB一致。结论5-Fu在诱导HCT116细胞凋亡的同时活化了NF-κB，uPA表达亦随之增强；PDTC在抑制5-Fu诱导的HCT116细胞NF-κB活化的同时增强了5-Fu诱导细胞凋亡的作用，uPA表达也相应下降

A study on the relationship among apoptosis , NF-κB activation and uPA expression of colon carcinama cell line induced by 5-fluorouracil

Abstract] Objectives To study the relationship among apoptosis , NF-κB activation and uPA expression in　human colon carcinama cell line HCT116 induced by 5-fluorouracil, and to oberve the effect of inhibited activity of NF-κB by PDTC on apoptosis as well as expression of uPA. Methods Cell apoptosis was analysed by Annexin Ⅴ-FITC.Fluctuation of NF-κB and uPA was detected by semi-quantitative immunohistochemistry. Results 5-fluorouracil could induce apoptosis and activate NF-κB .PDTC could significantly increased the apoptosis and suppressed the activation of NF-κB induced by 5-fluorouracil .The was a positive correlation between the changes of uPA and NF-κB. Conclusions 5-fluorouracil could induce apoptosis, activate NF-κB and up-regulate expression of uPA of HCT116 cells. The mechanism of enhanced apoptosis by PDTC may be related to suppressing activation of NF-κB and down-regulating expression of uPA.