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作 者:刘爱群[1] 余青云[1] 彭忠兴[1] 黄叶青[1] 刁胜朋[1] 程静[1] 王文涛[1] 洪铭范[1]
机构地区:[1]广东药学院附属第一医院神经内科,广东广州510008
出 处:《医学临床研究》2015年第7期1361-1363,共3页Journal of Clinical Research
摘 要:【目的】探讨miR-200c靶向调控DNA甲基转移酶1(DNMT1)对人胶质瘤U251细胞增殖的影响。【方法】采用实时荧光定量PCR(quantitative real—time PCR,qRT-PCR)检测24例胶质瘤组织和大脑正常组织中miR-200c与DNMT1的表达改变;将miR-200cmimics转染于胶质瘤U251细胞,以DNMT1 siRNA为阳性对照,采用qRT—PCR检测外源过表达miR-200c对DNMT1 mRNA表达水平的影响;采用MTT和法检测外源高表达miR-200c时胶质瘤U251细胞增殖能力的影响。【结果】qRT-PCR检测结果显示,miR-200c在24例胶质瘤组织中的表达水平较大脑正常组织明显下调,DNMT1在胶质瘤组织中的表达水平较大脑正常组织明显上调;外源过表达miR-200c下调胶质瘤U251细胞DNMT1mRNA的表达水平(P〈0.05),抑制胶质瘤U251细胞的生长(P〈0.05)。【结论】miR-200c通过靶向调控DNMT1抑制人胶质瘤细胞的增殖。[Objective] To explore whether miR-200c inhibits the proliferation of glioma cells through targeting DNMT1. [Methods] Quantitative real-time polymerase chain reaction (qRT-PCR) was employed for detecting the expressions of miR-200c and DNMT1 in glioma and normal brain specimens respectively, U251 cell was transfected with miR-200c mimics and DNMT1 si-RNA as a positive control. Then qRT-PCR was conducted for detecting the cellular expressions of DNMT1 mRNA regulated by miR-200c. And cell proliferation was assayed by methyl thiazolyl tetrazolium (MTT). [Results] miR-200c was down-regulated in glioma tissues while DNMT1 up-regulated in glioma tissues. The cellular level of DNMT1 mRNA was inhibited by restoring miR-200c or knocking down DNMT1. And an over-expression of miR-200c or a knock-down DNMT1 could inhibit the cell proliferation. [Conclusion] miR-200c inhibits cell proliferation through targeting DNMT1 in glioma ceils.
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