IL-24对氯化钴诱导缺氧乳腺癌细胞凋亡的影响  

Effect of IL-24 on Cell Apoptosis of Hypoxia Breast Cancer Induced by Cobalt Chloride

作　　者：王长文[1] 马洪波[1] 赵文秀[2] 

机构地区：[1]吉林医药学院公共卫生学院,吉林132013 [2]吉林医药学院药学院,吉林132013

出　　处：《吉林农业大学学报》2014年第3期310-313,318,共5页Journal of Jilin Agricultural University

基　　金：国家自然科学基金项目(82102953);吉林省中青年科技创新领军人才及团队项目(20130521018JH);吉林省教育厅"十二五"科学技术研究项目(2012496)

摘　　要：为研究IL-24对缺氧条件下诱导肿瘤细胞凋亡的影响。体外培养乳腺癌细胞,诱导化学缺氧模型后,转染IL-24基因,通过流式细胞术分析细胞周期和凋亡。结果表明:与对照组比较,缺氧诱导后的细胞增殖速度减慢。流式细胞术双染法分析细胞凋亡,可发现在缺氧生长条件下,IL-24基因转染可诱导乳腺癌细胞凋亡,相同时间点,细胞凋亡率无显著差异。转染IL-24基因后,缺氧和非缺氧小鼠乳腺癌细胞的红色荧光强度均随时间延长而下降。IL-24可通过内质网途径诱导缺氧以及非缺氧小鼠乳腺癌细胞发生凋亡。To analyze the effect of IL-24 on the induced tumor cell apoptosis under condition of hypoxia caused by cobalt chloride.Methods：The breast cancer cells were cultured in vitro and induced chemical anoxia models were set up.IL-24 gene transfection was carried out and cell apoptosis was analyzed by flow cytometry.The cell proliferation after hypoxia induction was slower compared with the control group.The breast cancer cell apoptosis happened after IL-24 genes transfection under condition of hypoxia by means of flow cytometry double staining.There was no significant difference of cell apoptosis rate at the same time point.The red fluorescence intensity of mouse breast cancer cells decreased with time under hypoxic and non-hypoxic conditions.IL-24 can induce the mouse breast cancer cell apoptosis under hypoxic and non-hypoxic conditions through the endoplasmic reticulum.

关 键 词：乳腺癌 IL-24基因 凋亡 氯化钴 缺氧 

分 类 号：R392.5[医药卫生—免疫学]