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miR-486对胶质瘤干细胞的抑制作用
作者姓名:周 静  张保朝
作者单位:南阳市中心医院神经内科,河南省南阳市 473000
摘    要:背景:既往研究发现,miR-486在胶质瘤干细胞(CD133+)中的表达水平显著低于其在胶质瘤非干细胞(CD133-)中的表达水平,但是miR-486对CD133+细胞的影响尚不明确。 目的:探索miR-486对CD133+细胞的作用。 方法:利用流式细胞分选将U87胶质瘤细胞中分为CD133+和CD133-细胞。通过脂质体转染构建miR-486过表达的胶质瘤干细胞。 结果与结论:流式细胞分选和纯化获得高比率的CD133+胶质瘤干细胞。实时反转录PCR检测发现miR-486在CD133+胶质瘤干细胞的表达水平比CD133-胶质瘤细胞明显下降。脂质体转染成功构建miR-486过表达的胶质瘤干细胞,体外实验发现miR-486高表达抑制胶质瘤干细胞的增殖,将其阻滞于G1/S期,并促进凋亡。提示miR-486对胶质瘤干细胞具有抑制作用。中国组织工程研究杂志出版内容重点:干细胞;骨髓干细胞;造血干细胞;脂肪干细胞;肿瘤干细胞;胚胎干细胞;脐带脐血干细胞;干细胞诱导;干细胞分化;组织工程

关 键 词:干细胞  肿瘤干细胞  胶质瘤干细胞  CmiRNA  miR-486  CD133+胶质瘤细胞  CD133-胶质瘤细胞  增殖  凋亡  细胞周期  

miR-486 is a tumor suppressor in glioma stem cells
Authors:Zhou Jing  Zhang Bao-chao
Institution:Department of Neurology, Central Hospital of Nanyang, Nanyang 473000, Henan Province, China
Abstract:BACKGROUND:Previous studies have found that the expression level of miR-486 in glioma stem cells (CD133+) is significantly down-regulated compared with that in glioma non-stem cells (CD133-), but the effect of down-regulation of miR-486 on CD133+ cells remains unclear . OBJECTIVE:To explore the effect of miR-486 on CD133+ cells. METHODS:CD133+ glioma stem cells and CD133- glioma cells were separated from U87 cells by flow cytometer. miR-486 overexpression glioma stem cells were constructed by lipofection transfection. RESULTS AND CONCLUSION:After sorting and purification, the content of the CD133+ fraction was enriched up to 83.5%. The expression level of miR-468 in CD133+ glioma stem cells was obviously down-regulated compared with that in CD133- glioma cells. CD133+ glioma stem cells overexpressing miR-486 were fabricated successfully. Results from in vitro experiments showed that miR-486 overexpression could dramatically decrease the proliferation of glioma stem cells, induce a cell cycle arrest in G1/S phase for CD133+ glioma stem cells and promote cell apoptosis. These findings suggest that miR-486 can be a suppressor of glioma stem cells, which offers a novel potential therapeutic target for glioma stem cells and human glioma.
Keywords:Brain Neoplasms  Glioma  MicroRNAs  Cell Cycle  Tissue Engineering  
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