miR-221/222 promote malignant progression of glioma through activation of the Akt pathway
miR-221/222 promote malignant progression of glioma through activation of the Akt pathway
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miR-221/222 通过激活 Akt 通路促进神经胶质瘤的恶性进展。
DOI：
10.3892/ijo_00000570
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发表时间：
2010-04-01
影响因子：
5.2
通讯作者：
Kang, Chunsheng
中科院分区：
文献类型：
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作者：
Zhang, Junxia;Han, Lei;Kang, Chunsheng
MicroRNAs （miRNAs）是一种短调控rna，在转录后水平负调控蛋白质表达。新出现的证据表明，mirna在几种癌症的发病机制中发挥重要作用。然而，miRNA的进一步机制尚不清楚。在本研究中，我们旨在通过生物信息学和实验方法探讨miR-221/222在胶质瘤中的协调功能。生物信息学分析显示，miR-221/222具有调控约70个常见靶基因的潜力，并可能通过Akt信号通路在调控和功能上发挥协同作用。在皮下小鼠模型中，过表达miR-221/222增加胶质瘤细胞的体外增殖和侵袭，并诱导胶质瘤生长。此外，miR-221/222过表达导致胶质瘤细胞中p-Akt明显活化，akt相关基因表达发生显著变化。我们的研究结果表明，miR-221/222通过调节常见基因表达介导的Akt通路激活，共同增强胶质瘤的恶性表型。
MicroRNAs (miRNAs) are short regulatory RNAs that negatively modulate protein expression at a post-transcriptional level. Emerging evidence suggests that miRNAs play important roles in the pathogenesis of several types of cancers. However, the further mechanisms of miRNA remain unknown. In this study, we aimed to explore the coordinated function of miR-221/222 in glioma by bioinformatics and experiment methods. Bioinformatics analysis revealed that miR-221/222 had the potential to regulate about 70 common target genes and may exert a cooperative effect on regulation and function via Akt signaling pathway. Overexpression of miR-221/222 increased glioma cell proliferation and invasion in vitro and induced glioma growth in a subcutaneous mouse model. Furthermore, miR-221/222 overexpression resulted in an obvious activation of p-Akt and significant changes of Akt-related gene expression in glioma cells. Our results suggest that miR-221/222 co-enhance the glioma malignant phenotype via activation of the Akt pathway mediated by regulation of common gene expression.