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作 者:张莉娟[1,2] 税青林[2] 彭春 何国平[3] 赵小平[2] 马莉[2]
机构地区:[1]江苏省无锡市妇幼保健院妇科 [2]四川省泸州医学院生物学与遗传学教研室,泸州646000 [3]四川大学华西医学院医学遗传学教研室,人类疾病基因组学研究室,人类疾病生物治疗教育部重点实验室
出 处:《肿瘤》2006年第1期17-20,共4页Tumor
基 金:四川省教育厅自然基金重点资助项目(编号:2002A068)
摘 要:目的研究c-myc反义寡核苷酸(ASODN)经脂质体LipfectAMINETM(LR)介导转染对MCF-7细胞中c-myc蛋白表达及细胞增殖、凋亡的影响。方法用四甲基偶氮唑盐法(MTT法)评价脂质体介导c-myc ASODN对细胞增殖的影响;免疫细胞化学ABC方法检测转染前后c-myc蛋白表达;流式细胞仪(FCM)定量分析细胞凋亡。结果ASODN/LR转染与正义、错义寡核苷酸相比,显著抑制MCF-7细胞增殖(P<0.01)。FCM分析结果显示,转染后可见明显细胞凋亡峰,72h相点细胞凋亡率达(28.76±2.09)%。免疫细胞化学显示c-myc蛋白水平明显降低,阳性表达率为(21.40±1.16)%。结论LR介导c-myc ASODN能明显抑制MCF-7细胞增殖、诱导细胞凋亡和下调c-myc蛋白水平。Objective: To investigate the effects of liposome (LipfectAMINETM, namely LR)-mediated c-myc antisense oligodeoxynucleotide(ASODN) on cell proliferation, c-myc protein expression, and apoptosis of MCF-7 cells. Methods: Cell proliferation was measured by MTT assay. Expression of c-myc protein was measured by immunocytochemistry before and after transfection. Apoptosis of cells was detected by flow cytometry. Results: Transfection of ASODN/LR markedly inhibited the proliferation of MCF-7 cells compared with sense and missense ODN( P〈0.01 ). FCM analysis showed that there appeared an obvious apoptosis peak after transfection. The apoptosis rate was maximum (28.76±2.09)% at 72 h. The immunocytochemistry staining showed that c-myc protein expression was suppressed significantly(21.4 ~ 1. 16)%. Conclusion: Liposome-mediated c-myc ASODN can evidently inhibit cell proliferation, down-regulate c-myc protein expression,and induce apoptosis of MCF-7 cells.
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