MiR-9通过抑制SMC1A表达促进GBM细胞系凋亡。

Yong Zu, Zhichuan Zhu, Min Lin, Dafeng Xu, Yongjun Liang, Yueqian Wang, Zhengdong Qiao, Ting Cao, Dan Yang, Lili Gao, Pengpeng Jin, Peng Zhang, Jianjun Fu, Jing Zheng
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引用次数: 10

摘要

目的:多形性胶质母细胞瘤(GBM)是恶性程度最高的脑癌,其基因组变异巨大,病理机制复杂。方法:MicroRNA通过靶向和调控蛋白质编码基因,是生物体内基因表达的精细转录后调节器。MiR-9被报道为GBM患者预后的重要生物标志物,也是GBM肿瘤干细胞调控的关键因素。为了探讨miR-9对GBM细胞生长的影响,我们在U87和U251细胞中过表达miR-9。miR-9过表达后,细胞活力下降,凋亡增加。为了确定miR-9的靶点,我们扫描了miR-9在表达SMC1A (1A染色体结构维持)基因的3'UTRs区域的结合位点,并设计了一种荧光报告试验来测量miR-9与该区域的结合。我们的研究结果显示,miR-9结合SMC1A的3'sUTR区域并下调SMC1A的表达。结果:我们的研究结果表明miR-9通过触发癌细胞凋亡是GBM的潜在治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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MiR-9 Promotes Apoptosis Via Suppressing SMC1A Expression in GBM Cell Lines.

Objective: Glioblastomas multiforme (GBM) is the most malignant brain cancer, which presented vast genomic variation with complicated pathologic mechanism.

Method: MicroRNA is a delicate post-transcriptional tuner of gene expression in the organisms by targeting and regulating protein coding genes. MiR-9 was reported as a significant biomarker for GBM patient prognosis and a key factor in regulation of GBM cancer stem cells. To explore the effect of miR-9 on GBM cell growth, we over expressed miR-9 in U87 and U251 cells. The cell viability decreased and apoptosis increased after miR-9 overexpression in these cells. To identify the target of miR-9, we scanned miR-9 binding site in the 3'UTRs region of expression SMC1A (structural maintenance of chromosomes 1A) genes and designed a fluorescent reporter assay to measure miR-9 binding to this region. Our results revealed that miR-9 binds to the 3'sUTR region of SMC1A and down-regulated SMC1A expression.

Result: Our results indicated that miR-9 was a potential therapeutic target for GBM through triggering apoptosis of cancer cells.

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