Department of Neurosurgery, The First Affiliated Hospital of Zhengzhou, No. 1, East Jianshe Road, Zhengzhou, Henan Province, China.
Department of Neurosurgery, The First Affiliated Hospital of Zhengzhou, No. 1, East Jianshe Road, Zhengzhou, Henan Province, China.
Biomed Pharmacother. 2017 Aug;92:690-695. doi: 10.1016/j.biopha.2017.05.096. Epub 2017 Jun 6.
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.
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.
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.
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.
异常的 DNA 甲基化与肿瘤的发生和发展有关。研究已经证实，miR-152 的 DNA 甲基化在许多肿瘤中受到介导，但它是否涉及神经胶质瘤仍不清楚。
本研究纳入了 20 名胶质瘤患者，分析 miR-152 的表达模式。实时 PCR 和 Western blot 分别用于检测 mRNA 或蛋白表达水平。通过荧光素酶报告实验检测 miR-152 与 runx2 之间的关系。通过甲基化特异性 PCR 测定 miR-152 的甲基化水平。通过 MTT 和 Annexin-FITC/PI 检测细胞增殖和凋亡。
miR-152 的表达在胶质瘤组织和细胞系中均下调，而 DNMT1 的表达上调。miR-152 在胶质瘤细胞系中呈高甲基化状态，其表达与 DNMT 呈负相关。DNMT1 敲低促进 miR-152 的表达，而 DNMT1 过表达则抑制 miR-152 的表达。miR-152 过表达促进神经胶质瘤细胞凋亡，而 miR-152 下调促进细胞增殖。miR-152 通过调控 Runx2 的表达来调节神经胶质瘤细胞的增殖和凋亡，而 miR-152 在神经胶质瘤组织和细胞中下调的机制是其高甲基化。
miR-152 通过 Runx2 调节神经胶质瘤的细胞增殖和凋亡，而 miR-152 在神经胶质瘤组织和细胞中下调的机制是其高甲基化。
