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      Decreased miRNA-637 is an unfavorable prognosis marker and promotes glioma cell growth, migration and invasion via direct targeting Akt1.

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          Abstract

          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, β-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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          Author and article information

          Journal
          Oncogene
          Oncogene
          1476-5594
          0950-9232
          Sep 17 2015
          : 34
          : 38
          Affiliations
          [1 ] Department of Neurosurgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.
          [2 ] Cancer Research Institute, Southern Medical University, Guangzhou, China.
          [3 ] Department of pathology, Basic School of Guangzhou Medical University, Guangzhou, China.
          [4 ] Department of Neurosurgery, the affiliated hospital of Luzhou medical college, Sichuan, China.
          [5 ] Cancer Center, TCM-Integrated Hospital of Southern Medical University, Guangzhou, China.
          Article
          onc2014419
          10.1038/onc.2014.419
          25597410
          a8eb692e-5358-4855-993d-26dd8784b87f
          History

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