Suppressing effect of atorvastatin on vasculogenic mimicry formation of gliomas
10.3760/cma.j.issn.1671-8925.2014.02.003
- VernacularTitle:阿托伐他汀对恶性胶质瘤血管生成拟态抑制作用的初步研究
- Author:
Shuyun HUANG
1
;
Xinlin SUN
;
Minjie LUO
;
Jianwen LI
;
Yiquan KE
Author Information
1. 510282 广州,南方医科大学珠江医院神经外科,广东神经外科研究所,广东省脑功能修复与再生重点实验室
- Keywords:
Glioma;
Vasculogenic mimicry;
Atorvastatin;
Matrix Metalloproteinase-2
- From:
Chinese Journal of Neuromedicine
2014;13(2):121-124
- CountryChina
- Language:Chinese
-
Abstract:
Objective To preliminarily explore the influence of intervention of atorvastatin in vasculogenic mimicry of glioblastoma and its mechanism.Methods CCK-8 experiment was carried out to detect the cell activity of glioma cell line U87 under the intervention of atorvastatin at different concentrations (1010-10-4 mol/L),aiming at screening out the safety concentration of atorvastatin.U87 cells were incubated in the mediums containing atorvastatin with different safety concentrations as well as in the control medium without atorvastatin.Three-D cultivation was performed in the Matrgel to establish the in vitro vasculogenic mimicry models,then the ability ofvasculogenic mimicry was observed and the length of the tube structure was counted.RT-PCR and Western blotting were performed to detect the mRNA and protein expression levels of matrix metalloproteinase-2 (MMP-2) in the U87 cells of intervention group and control group,respectively.Results Safety concentrations of atorvastatin screened by CCK-8 experiment were 10-7,10-6 and 10-5 mol/L.U87 cells formed the typical vasculogenic mimicry tube structure at 6-8 h after inoculation; the number of tube structure decreased with the increase ofatorvastatin concentration.Compared with the control group,the length counting of tube structure in intervention groups (10-7,10-6 and 10-5 mol/L) was significantly reduced and the mRNA and protein expression levels of MMP-2 were markedly decreased (P＜0.05).Conclusion Atovastatin significantly inhibits the vasculogenic mimicry formation via down-regulating the MMP-2 expression level.
