期刊
EXPERIMENTAL CELL RESEARCH
卷 320, 期 2, 页码 200-208出版社
ELSEVIER INC
DOI: 10.1016/j.yexcr.2013.10.020
关键词
MiR-26a; Glioblastoma multiforme; ATM; DNA repair
资金
- Shanghai Science and technology Committee [13XD1402600]
- Shanghai government [0952nm03900]
- Shanghai Jiao Tong University School of Medicine [BXJ201024]
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. (C) 2013 Elsevier Inc. All rights reserved.
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