Journal
CELL DEATH & DISEASE
Volume 11, Issue 9, Pages -Publisher
SPRINGERNATURE
DOI: 10.1038/s41419-020-02977-x
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Funding
- National Natural Science Foundation of China [81703041, 81502646, 81773354, 81872195]
- Joint Funds for the innovation of science and Technology, Fujian province [2017Y9050]
- Fujian provincial health and family planning research talent training program [2017-ZQN-30]
- Guangzhou Key Medical Discipline Construction Project
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Radiotherapy is one of the standard treatments for glioma patients; however, its clinical efficacy is limited by radioresistance. We identified a mechanism of such resistance mediated by linc-RA1 (radioresistance-associated long intergenic noncoding RNA 1). Linc-RA1 was upregulated in radioresistant glioma cells and glioma tissue samples, compared with radiosensitive cells and nontumor tissues. Linc-RA1 was associated with inferior overall survival and advanced clinical stage of glioma. Linc-RA1 promoted glioma radioresistance in vitro and in vivo. Mechanistically, linc-RA1 stabilized the level of H2B K120 monoubiquitination (H2Bub1) by combining with H2B and inhibiting the interaction between H2Bub1 and ubiquitin-specific protease 44 (USP44), which inhibited autophagy, thus contributing to glioma radioresistance. These results reveal that linc-RA1-mediated autophagy is a key mechanism of radioresistance and is an actionable target for improving radiotherapy efficacy in patients with glioma.
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