目的:探讨Racl、VEGF蛋白在肝细胞癌组织的表达及其与肿瘤血管形成的关系。方法:应用免疫组织化学法检测Racl、VEGF在43例肝细胞癌组织、43例癌旁肝组织及21例正常肝组织的表达,采用图像分析软件测定Racl蛋白、VEGF蛋白的平均光密度,根据CD34染色的血管内皮细胞计数肿瘤MVD。结果:Racl蛋白在癌组织、癌旁肝组织及正常肝组织均有表达,位于胞浆,癌组织表达高于癌旁肝组织(P〈O.01)、正常肝组织(P〈0.01);VEGF蛋白在癌组织、癌旁肝组织及正常肝组织均有表达,位于胞浆,癌组织高于癌旁肝组织(P〈O.01)、正常肝组织(P〈0.01);Racl、VEGF与MVD之间均呈正相关(r=O.490,P=0.001;r=0.355,P=0.019),Racl与VEGF之间呈正相关(r=0.583,P〈0.001)。结论:Racl可能通过上调VEGF的表达促进肿瘤血管生成,参与HCC的侵袭、转移机制。
Objective: This study aimed to detect Racl and vascular endothelial growth tactor (VEGF) expressions m nepatoceHuiar carcinoma (HCC) and to correlate this expression with tumor angiogenesis. Methods: Racl and VEGF expressions in 43 specimens of HCC, 43 specimens of adjacent nontumorous liver tissue, and 21 specimens of normal liver tissues were detected by immunohistochemistry. Image analysis software was used to conduct a quantitative analysis of Racl and VEGF expressions by accessing their mean optical density (MOD). Microvascular density (MVD) was determined by labeling the vascular endothelial cells with CD34. Results: Racl protein expression occurred mainly in the HCC tissue of the cytoplasm. MOD in HCC tissue was markedly higher than those in adjacent nontumorous liver tissue (P〈0.01) and in normal liver tissue (P〈0.01). The expression of VEGF protein was higher in HCC tissue than those in adjacent non-tumorous liver tissue (P〈0.01) and normal liver tissue (P〈0.01). Moreover, the Racl and VEGF protein expressions in HCC were positively correlated with MVD (r-0.490, P-0.001; r=0.355, P=0.019). Racl protein expression in HCC tissue was positively correlated with the VEGF protein expression in HCC tissue (r-0.583, P-0.000). Conclusion: Racl possibly promotes tumor angiogenesis through the upregulation of VEGF expression, and is associated with HCC invasion and metastasis.