p38MAPK信号通路影响血管内皮细胞生长因子诱导肝癌细胞超微结构变化  

Effect of p38MAPK signal pathway on ultrastructural change of liver cancer cells induced by VEGF

作　　者：毛华[1] 袁爱力[1] 赵敏芳 赖卓胜[1] 张亚历[1] 周殿元[1] 

机构地区：[1]中国人民解放军第一军医大学南方医院全军消化疾病研究所,广东省广州市510515 [2]珠江医院肿瘤中心

出　　处：《世界华人消化杂志》2000年第5期536-538,共3页World Chinese Journal of Digestology

摘　　要：目的研究 p38信号传导通路在血管内皮细胞生长因子(vascular endothdial growth factor,VEGF)诱导肝癌细胞超微结构变化中的作用.方法采用扫描电子显微镜观察 VEGF 以及预先用 SB203580特异性阻断 p38MAPK 信号传导通路后 VEGF 诱导肝癌细胞HepG_2形态学改变.结果扫描电镜显示肝癌细胞呈梭形,表面有细而稀疏的突起,VEGF 诱导后肝癌细胞成椭圆形,细胞表面伪足增多、变粗.阻断 p38MAPK 信号通路后,可抑制 VEGF 诱导的肝癌细胞表面伪足增多、变粗,促进肝癌细胞融合.结论 VEGF 通过 p38MAPK 信号通路诱导肝癌细胞伪足增多、变粗,降低细胞间粘附作用.AIM To study the effect of p38MAPK signal pathway on liver cancer cell's ultrastructural change induced by vascular endothelial growth factor (VEGF). METHODS Morphologic changes of liver carcinoma cells after being treated by VEGF and pretreated by a special inhibitor of p38MAPK SB203580 were observed under scanning electron microscope. RESULTS There were tiny and sparse pseudopodium on the liver carcinoma's surface which seemed shuttle in control group under scanning electron microscope.The cell became ellipse and there were more and thick pseudopodium in the cell surface after being treated by VEGF,which can be blocked by pretreatment with a special inhibitor of p38MAPK SB203580. CONCLUSION VEGF can promote more or thick pseudopodia on liver carcinoma cell surface by p38MAPK signal pathway,and decrease the adhesion among the cells.

关 键 词：细胞株 肝肿瘤 VEGF P38MAPK 

分 类 号：R735.7[医药卫生—肿瘤]