关键词: 血管生成拟态, 三氧化二砷, HepG2细胞；肝肿瘤

Abstract:

Abstract:Objective
To investigate the influence  of arsenic trioxide(AS2O3) in the vasculogenic mimicry(VM ) of HepG2 cells，and to preliminary clarify the possible mechanism of inhibition of AS2O3 on the VM.Methods The mean inhibitory concentration (IC50)  of AS2O3  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 IC50AS2O3 group and IC50 AS2O3 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 AS2O3 was 10 μmol•L^-1 72 h after reatment of HepG2 cells.The number,length and area of VM in 1/2 IC50 and IC50AS2O3 groups were significantly lower than those in control group (P<0.01); the number,length and area of VM in IC50AS2O3 group were also lower than those in 1/2 IC50AS2O3 group (P<0.05).Compared with control group,the expression levels of VE-cadherin and MMP-2 in 1/2 IC50 and IC50 AS2O3 groups were decre ased (P<0.05), and  the expression levels of caspase-3 and PCNA had no significant change (P>0.05).Conclusion AS2O3 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.

Key words: vasculogenic mimicry, arsenic trioxide, HepG2 cells, liver neoplasms