Role of microRNA-26b in glioma development and its mediated regulation on EphA2.
Role of microRNA-26b in glioma development and its mediated regulation on EphA2.
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DOI：
10.1371/journal.pone.0016264
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发表时间：
2011-01-14
期刊：
影响因子：
3.7
通讯作者：
Lin X
中科院分区：
文献类型：
--
作者：
Wu N;Zhao X;Liu M;Liu H;Yao W;Zhang Y;Cao S;Lin X
MicroRNAs(MiRNAs)是一种短的、非编码的RNA，调节多个靶基因的表达。MiRNAs的去调控在人类肿瘤发生中很常见。已发现miR-26b在胶质瘤细胞中低水平表达。然而，其潜在的作用机制尚未确定。实时定量聚合酶链式反应检测miR-26b在胶质瘤患者和细胞中的表达水平。MiR-26b水平与胶质瘤分级呈负相关。异位表达miR-26b抑制人脑胶质瘤细胞的增殖、迁移和侵袭。在EphA2的3‘非编码区中发现了miR-26b的结合位点。MiR-26b在胶质瘤细胞中的过表达抑制了EphA2蛋白的内源性水平。血管生成拟态实验进一步证实miR-26b对EphA2的调控作用，结果表明miR-26b抑制了EphA2调控的血管生成拟态过程。本研究表明miR-26b在脑胶质瘤中可能作为一种肿瘤抑制因子，直接调节EphA2的表达。EphA2是miR-26b的直接靶点，miR-26b对EphA2的下调依赖于miR-26b与EphA2基因3‘端非编码区microRNA的特异性反应元件的结合。
MicroRNAs (miRNAs) are short, non-coding RNAs that regulate the expression of multiple target genes. Deregulation of miRNAs is common in human tumorigenesis. Low level expression of miR-26b has been found in glioma cells. However, its underlying mechanism of action has not been determined. Real-time PCR was employed to measure the expression level of miR-26b in glioma patients and cells. The level of miR-26b was inversely correlated with the grade of glioma. Ectopic expression of miR-26b inhibited the proliferation, migration and invasion of human glioma cells. A binding site for miR-26b was identified in the 3′UTR of EphA2. Over-expression of miR-26b in glioma cells repressed the endogenous level of EphA2 protein. Vasculogenic mimicry (VM) experiments were performed to further confirm the effects of miR-26b on the regulation of EphA2, and the results showed that miR-26b inhibited the VM processes which regulated by EphA2. This study demonstrated that miR-26b may act as a tumor suppressor in glioma and it directly regulates EphA2 expression. EphA2 is a direct target of miR-26b, and the down-regulation of EphA2 mediated by miR-26b is dependent on the binding of miR-26b to a specific response element of microRNA in the 3′UTR region of EphA2 mRNA.
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影响因子：
14.9
作者：
Chen C;Ridzon DA;Broomer AJ;Zhou Z;Lee DH;Nguyen JT;Barbisin M;Xu NL;Mahuvakar VR;Andersen MR;Lao KQ;Livak KJ;Guegler KJ
通讯作者：
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影响因子：
6.2
作者：
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通讯作者：
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作者：
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通讯作者：
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影响因子：
10.5
作者：
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通讯作者：
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影响因子：
6.4
作者：
Miyazaki, T;Kato, H;Kuwano, H
通讯作者：
Kuwano, H