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作 者:陈烨[1] 缪金明[1] 朱学宏[1] 邵念贤[1] 方智雯[1] 欧阳仁荣[1]
机构地区:[1]上海第二医科大学附属仁济医院血液科
出 处:《中国肿瘤生物治疗杂志》2000年第1期56-59,共4页Chinese Journal of Cancer Biotherapy
基 金:国家自然科学基金!(39590291)资助
摘 要:目的:探讨抗PML-RARα反义核酸对早幼粒白血病细胞生长、细胞周期、细胞凋亡的作用。方法:以NB4细胞株为研究对象;细胞计数采用台盼兰排除、计数板计数法;白血病细胞集落采用甲基纤维素半固体培养;流式细胞仪(FCM)用于检测细胞凋亡和细胞周期。结果:以60μg/ml的终浓度处理细胞,抗 PML-RARα融合部位反义核酸(FUAS)能明显抑制NB4细胞增殖及白血病细胞集落(AML-CFU)形成,最大抑制率分别为46.8%,51.6%;GM-CSF能减弱FUAS的作用,FUAS作用时间越短,GM-CSF促AML-CFU增加越明显;FUAS处理第7,9天,出现明显的凋亡细胞群,凋亡细胞百分比分别为41.0%,34.2%;FUAS处理第5天S期下降,G2/M期升高,第7天C0/G1期明显升高,S期回升。结论:抗PML-RARα反义核酸具有抑制早幼粒白血病细胞增殖、诱导细胞凋亡的作用。Objective: To investigate the effects of PML-RARαantisense on the growth, cell cycle and apoptosis of NB4 cells. Methods: Cell apoptosis and cell cycle were detected by flow cytometry, and leukemic colony forming unit was exammed by methylcellulose assays. Results: PML-RARα antisence (FUAS) could inhibited the growth, and formation of acute myelocytic leukemia colony forming unit (AML-CFU)in NB4 cells; GM-CSF could enhance AML-CFU formation and antagonized the effect of FUAS on AML-CFU formation inhibition. The shorter the time of incubation with FUAS was, the more markedly GM-CSF en- hanced the AML-CFU formation. At 7 days, 9 days of treatment with FUAS percentage of apoptotic cells was 41. 5 %, 34. 2% respectively. Reduction of S phase and increase of G2/M Phase at 5 days, significant increase of G0/G1 Phase with S phase at 7 days. Conclusion: PMLRARα antisence can inhibit the cell growth and induce cell apoptosis of NB4 cells.
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