期刊
NEUROSCIENCE LETTERS
卷 590, 期 -, 页码 40-46出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2015.01.060
关键词
Glioblastoma; miR-29 family; DNA methyltransferase; Proliferation; Invasion; Apoptosis
资金
- National Basic Research Program of China (973 Program) [2010CB529405]
- National Natural Science Foundation of China [81202102, 81402050]
- Ph.D. Program Foundation of Ministry of Education of China [20121202120018]
- Science and Technology Commission Foundation of Tianjin Municipal [12ZCDZSY17400, 13JCQNJC12100]
- Foundation of Tianjin Municipal Education Commission [2004ZD06, 20110102]
- Foundation of Chinese Neuro-Oncology Society [CSNO-2013-MSD010]
- Foundation of Tianjin Medical University [2013KYQ02]
miR-29s (including miR-29a-c) have been confirmed to be effective tumor suppressors for a variety of malignant tumors including glioblastoma. Promoter hypermethylation resulting from DNMT3A and 3B overexpression is an important epigenetic mechanism for tumor suppressive gene silencing. Bioinformatics predicts both DNMT3A and 3B are targets of miR-29s, but the anti-glioblastoma effects of miR-29s induced DNMT3A/3B downregulation deserve further investigation. We herein demonstrated that miR-29s effectively blocked DNMT3A and 3B expression by degrading their mRNAs in U87MG glioblastoma cell line. Exogenous miR-29s substantially inhibited the proliferation, migration and invasion of U87MG cells, and promoted their apoptosis. These effects could be perfectly mimicked by a small interfering RNA against DNMT3A and 3B, and partially compromised by DNMT3A/3B expression plasmids co-transfection, suggesting that miR-29s exerted the above tumor suppressive effects at least partly by silencing DNMT3A/3B. These findings provide a rationale for miR-29s based therapeutic strategies against glioblastoma. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
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