Backgrounds and aims: Glioma accounts for the majority of primary malignant brain tumors in adults. Upregulation of microRNA-26a (miR-26a) has been observed in glioma. However, the biological function and molecular mechanism of miR-26a in glioma remain to be elucidated.
Methods: Glioma cells stably overexpressing or down-expressing miR-26a were analyzed for both in vitro and in vivo biological functions. Novel target of miR-26a was identified by bioinformatics searching and molecular biological assays. Glioma specimens and normal brain tissues were analyzed for both expression levels of miR-26a and its target.
Results: Forced expression of miR-26a in glioma cells significantly increased both growth rate and colony formation in vitro and tumor growth and angiogenesis in vivo, while reduced expression of miR-26a played opposite roles. MiR-26a directly targeted prohibitin (PHB) whose expression levels were downregulated in glioma specimens. The levels of miR-26a were inversely correlated with PHB expression levels in glioma samples and strongly correlated with clinical WHO grades of glioma.
Conclusion: These results reveal that miR-26a regulates PHB and promotes glioma progression both in vitro and in vivo and that miR-26a and its target PHB are associated with glioma development, which can be helpful in developing microRNA-based treatment for glioma in the future.
Keywords: Angiogenesis; Glioma; MicroRNA-26a; Prohibitin; Tumor growth.
© 2013 John Wiley & Sons Ltd.