Expression and function of miR-27b in human glioma

Expression and function of miR-27b in human glioma
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miR-27b在人胶质瘤中的表达和功能

DOI:
10.3892/or.2011.1458
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发表时间:
2011-12-01
期刊:
影响因子:
4.2
通讯作者:
Kang, Chunsheng
Kang, Chunsheng
中科院分区:
医学3区
文献类型:
--
作者:
Chen, Lingchao;Li, Huibing;Kang, Chunsheng

文献摘要

被引文献

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我们先前的miRNAs谱研究显示,与H4低级别星形细胞瘤细胞相比,miR-27 b在胶质瘤细胞中上调。然而,miR-27 b在胶质瘤中的主要功能尚不清楚。本研究旨在探讨miR-27 b在胶质瘤中的表达及其在胶质瘤发病机制中的作用。Real-time PCR结果显示,miR-27 b在胶质瘤标本和胶质瘤细胞中表达上调。下调miR-27 b可抑制胶质瘤细胞的生长、诱导细胞凋亡并抑制其侵袭。此外,TOPflash荧光素酶活性显著降低,而FOPflash荧光素酶没有显著变化。Western blot结果显示,miR-27 b抑制剂可下调STAT 3、c-myc和cyclin D1的表达。这些发现表明,异常上调的miR-27 b可能是导致人类胶质瘤恶性的关键因素之一。
Our previous miRNAs profiling study showed that miR-27b was up-regulated in glioma cells compared with H4 low grade astrocytoma cells. However, the main function of miR-27b in glioma in not known yet. The aim of this study was to investigate the expression and function of miR-27b in the pathogenesis of glioma. Real-time PCR showed that miR-27b was up-regulated in glioma samples and glioma cells. Downregulation of miR-27b triggered growth inhibition, induced apoptosis and inhibited invasion in glioma cells. Furthermore, TOPflash luciferase activity was decreased significantly, while FOPflash luciferase did not change significantly. In addition, Western blot assay showed that STAT3, c-myc and cyclin D1 were knocked down after treatment with miR-27b inhibitor. These findings suggest that aberrantly up-regulated miR-27b may be one of the critical factors that contribute to malignancy in human gliomas.