Journal
ONCOGENE
Volume 34, Issue 38, Pages 4952-4963Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2014.419
Keywords
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Funding
- National Nature Science Fund of China [81372692]
- Natural Science Fund of Guangdong Province [S2013010014886]
- Medical Scientific Research Fund of Guangdong Province [B2013238]
- Scientific Research Initiative Project Fund of Southern Medical University [B1012032]
- President Fund of Nanfang Hospital [2011C007, 2012C011]
- Science Fund of the Affiliated Hospital of Luzhou Medical College [2013-60]
- Science and Technology Project of Luzhou [3-S-48]
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Although increasing evidence indicated that the deregulation of microRNAs (miRNAs) contributes to tumorigenesis and invasion, little is known about the role of miR-637 in human gliomas. In the present study, we found that the expression level of miR-637 was significantly reduced in clinical glioma tissues compared with normal brain tissues. Moreover, we revealed that the introduction of miR-637 dramatically suppressed glioma cell growth, migration and invasion in vitro and in vivo. Further studies revealed that Akt1 is a direct target gene of miR-637. Silencing of Akt1 inhibited the growth and invasion of glioma cells by decreasing phosphorylated Akt, beta-catenin, phosphorylated Foxo1 and Cyclin D1 and inducing the expression of Foxo1, which was consistent with the effect of miR-637 overexpression. Suppressed expression of miR-637 and increased Akt1 protein levels were correlated with unfavorable progression and poor prognosis, respectively, and a negative relationship between the miR-637 expression and Akt1 protein levels was observed in gliomas. Our findings provide new insights into the role of miR-637 in the development of gliomas, and implicate the potential application of miR-637 in cancer therapy.
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