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

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.