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Highlights: [•] The c-Myc oncogene directly upregulates miR-26a expression in GBM cells. [•] ChIP assays demonstrate that c-Myc interacts with the miR-26a promoter. [•] Luciferase reporter assays show that PTEN is a specific target of miR-26a. [•] C-Myc–miR-26a suppression of PTEN may regulate the PTEN/AKT pathway. [•] Overexpression of c-Myc enhances the proliferative capacity of GBM cells. [ABSTRACT FROM AUTHOR]

Abstract: Glioblastoma multiforme (GBM) is notoriously resistant to radiation, and consequently, new radiosensitizers are urgently needed. MicroRNAs are a class of endogenous gene modulators with emerging roles in DNA repair. We found that overexpression of miR-26a can enhance radiosensitivity and reduce the DNA repair ability of U87 cells. However, knockdown miR-26a in U87 cells could act the converse manner. Mechanistically, this effect is mediated by direct targeting of miR-26a to the 3′UTR of ATM, which leads to reduced ATM levels and consequent inhibition of the homologous recombination repair pathway. These results suggest that miR-26a may act as a new radiosensitizer of GBM. [Copyright &y& Elsevier]