血管内皮生长因子受体-1对肝癌侵袭转移的影响

目的 通过检测血管内皮生长因子受体-1(vascular endothelial growth factor receptor-1,VEGFR-1)在肝癌组织中的表达,探讨VEGFR-1在肝癌侵袭、转移中的作用.方法 共取82例肝癌组织和癌旁肝组织的石蜡标本,采用免疫组织化学方法检测VEGFR-1、上皮标志物E-钙黏蛋白和间叶标志物波形蛋白的表达情况,并分析其关系.对肝癌患者临床病理学指标和HBV感染中VEGFR-1的表达进行分析.结果 癌旁肝组织中无VEGFR-1表达,肝癌组织中VEGFR-1的表达率为89%(73/82).VEGFR-1的表达在肿瘤分期、门静脉癌栓、肿瘤包膜、肿瘤直径、分化程度差异有统计学意义(x2=22.192,15.934,16.751,20.154,6.487,P＜0.05);对术后1、2年的复发率和术后2年生存率有影响(x2=0.983,0.958,0.847,P＜0.05);对术后1年的生存率无影响(x2=0.359,P＞0.05).VEGFR-1与E-钙黏蛋白的表达呈负相关(r=0.765,P＜0.01),而与波形蛋白的表达呈正相关(r=1.469,P＞0.05).结论 VEGFR-1可能在肝癌的侵袭、转移中发挥作用,其促肝癌侵袭转移可能与肝癌细胞发生上皮-间叶样表型转化有关.

Effects of vascular endothelial growth factor receptor-1 on the invasion and metastasis of hepatocellular carcinoma

Objective To investigate the effects of vascular endothelial growth factor receptor-1(VEGFR-1) in the invasion and metastasis of hepatocellular carcinoma(HCC)by detecting the expression of VEGFR-1 in HCC tissues.Methods Paraffin-embedded tissue which containing HCC tissues and adjacent tissues were prepared from patients(n=82)with HCC,then were analyzed by immunohistochemical technique for the expression of VEGFR-1,epithelial marker E-cadherin and mesenchymal marker Vimentin.The relationship between the expression of VEGFR-1 and pathological parameters,and the correlation between VEGFR-1 and E-cadherin,VEGFR-1 and Vimentin were analyzed.Results The expression rates of VEGFR-1 in HCC tissues and adjacent tissues were 89%(73/82)and 0,respectively.The difference of VEGFR-1 expression in portal vein tumor thrombus,tumor capsule,stage,size and differentiation grade of tumor had statistical significance(x2=22.192,15.934,16.751,20.154,6.487,P＜0.05).The expression of VEGFR-1 had effect on the 1-,2-year recurrence rate and 2-year survival rate (x2=0.983,0.958,0.847,P＜0.05),but not on 1-year survival rate(x2=0.359,P＞0.05).The expression of VEGFR-1 was negatively correlated with that of E-cadherin(r=0.765,P＜0.01)but positively with that of Vimentin (r=1.469,P＞0.05).Conclusions VEGFR-1 may play an important role in invasion and metastasis of HCC.Epithelial-mesenehymal transition that induced by VEGFR-1 may contribute to the invasion and metastasis of HCC.