1. MiR-26a enhances the radiosensitivity of glioblastoma multiforme cells through targeting of ataxia-telangiectasia mutated.
- Author
-
Guo P, Lan J, Ge J, Nie Q, Guo L, Qiu Y, and Mao Q
- Subjects
- Animals, DNA Repair genetics, DNA Repair radiation effects, Gene Expression Regulation, Neoplastic, Gene Knockdown Techniques, Gene Targeting, Humans, Mice, Mice, Nude, MicroRNAs antagonists & inhibitors, Tumor Cells, Cultured, Xenograft Model Antitumor Assays, Ataxia Telangiectasia Mutated Proteins genetics, Brain Neoplasms genetics, Brain Neoplasms radiotherapy, Glioblastoma genetics, Glioblastoma radiotherapy, MicroRNAs physiology, Radiation Tolerance genetics
- 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., (© 2013 The Authors. Published by Elsevier Inc. All rights reserved.)
- Published
- 2014
- Full Text
- View/download PDF