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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

宋海林 王雪雯 段晶晶 周明 杨莉

吉林大学学报(医学版)Issue(4):715-719,5.
吉林大学学报(医学版)Issue(4):715-719,5.DOI:10.13481/j.1671-587x.20140404

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

Influence of arsenic trioxide in vasculogenic mimicry of HepG2 cells and its mechanism

宋海林 1王雪雯 1段晶晶 1周明 1杨莉1

作者信息

  • 1. 石河子大学医学院病理生理学教研室,新疆地方与民族高发病教育部重点实验室,新疆 石河子 832002
  • 折叠

摘要

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&nbsp;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 .

关键词

血管生成拟态/三氧化二砷/HepG2 细胞/肝肿瘤

Key words

vasculogenic mimicry/arsenic trioxide/HepG2 cells/liver neoplasms

分类

医药卫生

引用本文复制引用

宋海林,王雪雯,段晶晶,周明,杨莉..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[J].吉林大学学报(医学版),2014,(4):715-719,5.

基金项目

国家自然科学基金资助课题 ()

吉林大学学报(医学版)

OA北大核心CSCDCSTPCD

1671-587X

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