MiR-26a enhances the radiosensitivity of glioblastoma multiforme cells through targeting of ataxia-telangiectasia mutated.
Exp Cell Res
; 320(2): 200-8, 2014 Jan 15.
Article
in En
| MEDLINE
| ID: mdl-24211747
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.
Key words
Full text:
1
Database:
MEDLINE
Main subject:
Radiation Tolerance
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Brain Neoplasms
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Glioblastoma
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MicroRNAs
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Ataxia Telangiectasia Mutated Proteins
Limits:
Animals
/
Humans
Language:
En
Year:
2014
Type:
Article