Methylation mediated silencing of miR-23b expression and its role in glioma stem cells

► It is the first time to report that miR-23b was silenced mediated by hypermethylation in GSCs. ► The expression level of miR-23b is lower in U87 GSCs when compared with parallel U87 cells. ► miR-23b induced U87 GSCs’ cell-cycle arrest and proliferation inhibition. ► miR-23b enhances the sensitivit...

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Bibliographic Details
Published in:Neuroscience letters 2012-10, Vol.528 (2), p.185-189
Main Authors: Geng, Jiong, Luo, Hui, Pu, Yi, Zhou, Zhimin, Wu, Xiaoming, Xu, Wenhui, Yang, Zhengxiang
Format: Article
Language:English
Subjects:
Antineoplastic Agents - pharmacology
Azacitidine - analogs & derivatives
Azacitidine - pharmacology
Brain Neoplasms
Cell Cycle Checkpoints
Cell Line, Tumor
Cell Proliferation
Dacarbazine - analogs & derivatives
Dacarbazine - pharmacology
Down-Regulation
Epigenesis, Genetic
Gene Silencing
Glioma
Glioma stem cells
Humans
Indexing in process
Methylation
MicroRNA
MicroRNAs - genetics
MicroRNAs - metabolism
Neoplastic Stem Cells - drug effects
Neoplastic Stem Cells - metabolism
Promoter Regions, Genetic
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Summary:► It is the first time to report that miR-23b was silenced mediated by hypermethylation in GSCs. ► The expression level of miR-23b is lower in U87 GSCs when compared with parallel U87 cells. ► miR-23b induced U87 GSCs’ cell-cycle arrest and proliferation inhibition. ► miR-23b enhances the sensitivity of U87 GSCs to TMZ. MicroRNAs (miRNAs) are a class of small non-coding RNAs that negatively regulate gene expression at a post-transcriptional level. Some miRNAs harboring CGIs undergo methylation mediated silencing, a characteristic of many tumor suppressor genes. To identify such miRNAs in glioma stem cells (GSCs), we first showed that miR-23b is frequently methylated in GSCs but not in parallel U87 cells. Meanwhile, miR-23b expression was also markedly reduced in GSCs compared with matching U87 cells. Furthermore, treatment with 5-aza can increase miR-23b expression in GSCs. In addition, ectopic expression of miR-23b in GSCs induces cell cycle arrest and proliferation inhibition. Further analysis showed that miR-23b could enhance the sensitivity of U87 GSCs to TMZ. Our results suggest that miR-23b is epigenetically down-regulated and restoration of miR-23b can effectively suppress cell growth in GSCs.
ISSN:0304-3940
1872-7972
DOI:10.1016/j.neulet.2012.08.055