1. miR-152 regulated glioma cell proliferation and apoptosis via Runx2 mediated by DNMT1.
- Author
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Zhang P, Sun H, Yang B, Luo W, Liu Z, Wang J, and Zuo Y
- Subjects
- Cell Line, Tumor, Core Binding Factor Alpha 1 Subunit genetics, DNA (Cytosine-5-)-Methyltransferase 1 genetics, Glioma genetics, Humans, Apoptosis physiology, Cell Proliferation physiology, Core Binding Factor Alpha 1 Subunit biosynthesis, DNA (Cytosine-5-)-Methyltransferase 1 biosynthesis, Glioma metabolism, MicroRNAs physiology
- Abstract
Background: Aberrant DNA methylation is associated with tumor onset and progression. Study has verified that the DNA methylation of miR-152 was mediated in many tumors, but whether it involved in glioblastomas was still unclear., Methods: This study enrolled 20 patients with glioma to analyze the expression pattern of miR-152. Real-time PCR and western blot were used to detect the mRNA or protein expression level, respectively. The relationship between miR-152 and runx2 was detected by Luciferase reporter assay. The methylation level of miR-152 was determined by methylation-specific PCR. Cell proliferation and apoptosis were detected by MTT and Annexin-FITC/PI assay., Results: The expression of miR-152 was down-regulated while the expression of DNMT1 was up-regulated in both glioma tissue and cell lines. MiR-152 was hypermethylated and its expression was negatively correlated with DNMT in glioma cell lines. DNMT1 knockdown promoted the expression of miR-152, however, DNMT1 overexpression suppressed the expression of miR-152. MiR-152 overexpression promoted glioma cell apoptosis while miR-152 knockdown promoted cell proliferation. MiR-152 targets Runx2 to regulate its expression, Runx2 overexpression abolished the effects of miR-152 overexpression., Conclusion: MiR-152 regulated cell proliferation and apoptosis of glioma mediated by Runx2, while the mechanism of down regulated miR-152 in glioma tissues and cells was its hypermethylation., (Copyright © 2017 Elsevier Masson SAS. All rights reserved.)
- Published
- 2017
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