Influence of arsenic trioxide in vasculogenic mimicry of HepG2 cells and its mechanism
10.13481/j.1671-587x.20140404
- VernacularTitle:三氧化二砷对肝癌HepG2细胞形成血管生成拟态的影响及其机制
- Author:
Hailin SONG
;
Xuewen WANG
;
Jingjing DUAN
;
Ming ZHOU
;
Li YANG
- Publication Type:Journal Article
- Keywords:
vasculogenic mimicry;
arsenic trioxide;
HepG2 cells;
liver neoplasms
- From:
Journal of Jilin University(Medicine Edition)
2014;(4):715-719
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the influence of arsenic trioxide (AS2 O3 )in the vasculogenic mimicry (VM ) of HepG2 cells, and to preliminary clarify the possible mechanism of inhibition of AS2 O3 on the VM. Methods Themean inhibitory concentration (IC50 )of AS2 O3 72 h after treatment of HepG2 cells was calculated by CCK-8 assay.The HepG2 cells were cultured on 3-D Matrigel and randomly divided into control group, 1/2 IC50 AS2 O3 group and IC50 AS2 O3 group.IPP software was used to calculate the number,length and area of VM,and the expression levels of VM-related proteins VE-cadherin and MMP-2, apoptotic-related protein caspase-3 and proliferation-related protein PCNA were detected by Western blotting method.Results The IC50 of AS2 O3 was 10μmol·L-1 72 h after treatment of HepG2 cells.The number,length and area of VM in 1/2 IC50 and IC50 AS2 O3 groups were significantly lower than those in control group (P<0.01);the number,length and area of VM in IC50 AS2 O3 group were also lower than those in 1/2 IC50 AS2 O3 group (P<0.05).Compared with control group,the expression levels of VE-cadherin and MMP-2 in 1/2 IC50 and IC50 AS2 O3 groups were decreased (P<0.05),and the expression levels of caspase-3 and PCNA had no significant change (P>0.05).Conclusion AS2 O3 can inhibit the forming of VM of HepG2 cells,which indicated that its mechanism may be related to inhibiting the expressions of VE-cadherin and MMP-2 .
