miR-152 regulated glioma cell proliferation and apoptosis via Runx2 mediated by DNMT1 - 01/07/17
, Hongwei Sun, Bo Yang, Wenzheng Luo, Zengjin Liu, Junkuan Wang, Yuchao ZuoBienvenue sur EM-consulte, la référence des professionnels de santé.
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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.
Le texte complet de cet article est disponible en PDF.Keywords : Glioma, miR-152, Methylation, Runx2, Apoptosis
Plan
Vol 92
P. 690-695 - août 2017 Retour au numéro
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