MiR-24反义核酸通过BIM-Smac/Diablo途径促进多柔比星对结肠癌细胞的凋亡诱导效应

被引:6
作者
徐烨
崔焌辉
陈诚豪
都志军
机构
[1] 浙江省立同德医院肛肠科
关键词
miR-24; BIM; Smac/DIABLO; SW480; 多柔比星;
D O I
10.13748/j.cnki.issn1007-7693.2016.02.010
中图分类号
R735.35 [];
学科分类号
摘要
目的探讨miR-24在结肠癌中发挥的作用并研究其是否和多柔比星的体外治疗有关。方法用RT-q PCR法检测miR-24在结肠癌患者血浆中及结肠癌细胞系中的表达水平。MTT法检测miR-24反义核酸对多柔比星杀伤结肠癌细胞能力的影响。利用生物信息学、定量PCR及Western blot法验证miR-24是否调节结肠癌细胞BIM的表达。运用JC-1染色、Annexin V染色及Western blot法研究miR-24反义核酸影响多柔比星疗效的信号通路。结果结肠癌患者血浆及结肠癌细胞系中miR-24表达水平显著升高。miR-24反义核酸可显著增强多柔比星对SW480细胞的杀伤活性。定量PCR及Western blot实验表明miR-24的靶基因可能为BIM。miR-24反义核酸联合多柔比星可引起SW480细胞线粒体膜电位的丧失并诱导线粒体内Smac/DIABLO的释放,进而引起caspase-3的活化和凋亡的发生。转染BIM si RNA后miR-24反义核酸联合多柔比星对SW480细胞的凋亡诱导效应显著降低。结论 Mi R-24反义核酸通过BIM-Smac/Diablo途径促进多柔比星对结肠癌细胞的凋亡诱导效应。
引用
收藏
页码:175 / 181
页数:7
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