Role of miR-613 as a tumor suppressor in glioma cells by targeting SOX9
Authors Sang Q, Liu X, Sun D
Received 9 November 2017
Accepted for publication 24 January 2018
Published 30 April 2018 Volume 2018:11 Pages 2429—2438
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Amy Norman
Peer reviewer comments 2
Editor who approved publication: Dr Yao Dai
Qiuling Sang,1 Xuejuan Liu,2 Daju Sun3
1Department of Neurology, The China–Japan Union Hospital of Jilin University, Changchun, People’s Republic of China; 2Department of Pathology, The First Hospital of Jilin University, Changchun, People’s Republic of China; 3Department of Pathology, The China–Japan Union Hospital of Jilin University, Changchun, People’s Republic of China
Background and objectives: MicroRNA-613 (miR-613), a novel cancer-related microRNA, has been shown to be responsible for the inhibition of tumor development and progression in various cancers. We aimed to investigate the biological function and regulatory mechanisms of miR-613 in gliomas.
Materials and methods: miR-613 expression were detected by qRT-PCR assays in glioma tissues and cell lines. Cell Counting Kit-8 (CCK-8) assay, colony formation analysis, wound healing and transwell invasion assays were performed to evaluate cell proliferation, colony formation, migration and invasion abilities. Luciferase reporter assays, qRT-PCR and Western blot were performed to explore the potential targets of miR-613. Xenograft mice model was established to evaluate the effect of miR-613 in vivo.
Result: The expression levels of miR-613 were significantly downregulated in the glioma tissues and cell lines, and the decreased level was significantly negatively associated with the overall disease-free survival of the patients. Functionally, ectopic expression of miR-613 in glioma cells suppressed the proliferation, colony formation, and migration and invasion of the cells. The sex-determining region Y-box 9 (SOX9) was identified as a direct functional target of miR-613, and its expression was inversely correlated with miR-613 expression in glioma tissues. Moreover, rescue of SOX9 could partially reverse the inhibitory effects of miR-613 on glioma cell proliferation, colony formation, migration, and invasion. Importantly, miR-613 also suppressed tumor growth in vivo by targeting SOX9.
Conclusion: Taken together, these findings demonstrate that miR-613 functions as a tumor suppressor in glioma cells by directly targeting SOX9.
Keywords: miR-613, glioma, SOX9, proliferation, invasion
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