| Literature DB >> 25625222 |
Hui Xu1, Jing Sun1, Cuijuan Shi1, Cuiyun Sun1, Lin Yu2, Yanjun Wen1, Shujun Zhao3, Jing Liu1, Jinling Xu1, Huining Li1, Tongling An1, Xuexia Zhou1, Linlin Ren1, Qian Wang4, Shizhu Yu5.
Abstract
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.Entities:
Keywords: Apoptosis; DNA methyltransferase; Glioblastoma; Invasion; Proliferation; miR-29 family
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Year: 2015 PMID: 25625222 DOI: 10.1016/j.neulet.2015.01.060
Source DB: PubMed Journal: Neurosci Lett ISSN: 0304-3940 Impact factor: 3.046