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作 者:蔡辉[1] 马云涛[1] 苏河[1] 郭天康[1] 李振军[1]
出 处:《兰州大学学报(医学版)》2007年第1期26-29,共4页Journal of Lanzhou University(Medical Sciences)
基 金:甘肃省中青年科技基金(3YS061-A25-025)资助项目。
摘 要:目的观察c-myc反义寡核苷酸对胃癌MKN-45细胞株增殖的抑制作用。方法用四甲基偶氮唑盐法评价脂质体介导c-myc反义寡核苷酸对细胞增殖的影响,免疫细胞化学ABC方法检测转染后c-myc蛋白表达;荧光显微镜观察细胞凋亡;流式细胞仪分析细胞凋亡。结果c-myc基因反义寡核苷酸转染MKN-45细胞后,可以显著抑制细胞增殖,其抑制作用具有剂量依赖性;流式细胞仪分析结果显示,转染后能诱导胃癌细胞凋亡,G_0/G_1期细胞增多;免疫细胞化学显示c-myc蛋白水平明显降低,阳性表达率为64.9%±5.68%。结论c-myc基因反义寡核苷酸能明显抑制胃癌MKN-45细胞增殖、诱导细胞凋亡和下调c-myc蛋白水平。Objective To observe the inhibitory effects of c-myc antisense oligonucleotides on the proliferation of MKN-45 cells. Methods Cell proliferation was measured by MTT assay. Expression of c-myc protein was measured by immunocytochemistry after transfection. Apoptosis of cells was detected by flow cytometry and fluorescence microscope. Results After sealing c-myc gene with ASODN, the proliferation of MKN-45 cells was inhibited markedly. FCM analysis showed that an obvious apoptosis peak appeared after transfection. The immunocytochemistry staining showed that c-myc protein expression was suppressed significantly 64.9%±5.68%. Conclusion Liposome-mediated c-myc ASODN can evidently inhibit cell proliferation, down-regulate c-myc protein expression, and induce apoptosis of MKN-45 cells.
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