Caveolin-1在肝细胞癌表达及与肿瘤血管生成的关系

目的：探讨caveolin-1与肝细胞癌（HCC）侵袭转移的关系及其可能的机制。方法：应用实时PCR方法检测伴肝内转移的 HCC组织、癌旁组织、肝硬化组织、正常肝组织中 caveolin-1 mRNA的表达；用Western blot方法检测伴肝内转移的 HCC组织、癌旁组织中caveolin-1蛋白的表达；用免疫组化方法检测75例HCC组织中caveolin-1，血管内皮生长因子（VEGF），CD34，α-平滑肌肌动蛋白（α-SMA）的表达，分析caveolin-1，VEGF的表达以及肿瘤微血管密度（MVD），非成对动脉（UA）计数与临床病理因素的关系。结果：在伴肝内转移的HCC组织中，caveolin-1 mRNA表达明显高于癌旁组织、肝硬化组织、正常肝组织（均P<0.05），其蛋白表达明显高于癌旁组织；caveolin-1表达水平的升高与肿瘤转移有关（P<0.05），且caveolin-1的表达与VEGF表达及MVD和UA计数呈正相关（r=0.293，P=0.011；r=0.361，P=0.001；r=0.388，P=0.001）。结论：caveolin-1表达升高促进HCC的侵袭转移，其机制可能是通过诱导HCC表达VEGF，促进肿瘤新生血管生成而实现的。

Expression of caveolin-1 in hepatocellular carcinoma and its relation with tumor angiogenesis

Objective: To investigate the relation of caveolin-1 with invasion and metastasis of hepatocellular carcinoma (HCC) and possible underlying mechanism. Methods: The caveolin-1 mRNA expressions in the tumor tissues from HCC patients with intrahepatic metastasis and their adjacent tissues, as well as cirrhosis and normal liver tissues were detected by real-time PCR method. The caveolin-1 protein expressions in the tumor tissues from HCC patients with intrahepatic metastasis and their adjacent tissues were determined by Western blot analysis. Immunohistochemical staining was performed on the HCC specimens from 75 HCC cases to detect the expression of caveolin-1, vascular endothelial growth factor (VEGF), CD34 and α-smooth muscle actin (α-SMA), and then the relations of caveolin-1, VEGF, microvessel density (MVD) and unpaired artery (UA) with the clinicopathological factors of HCC patients were analyzed. Results: Of the HCC patients with intrahepatic metastasis, the expression level of caveolin-1 mRNA in tumor tissues was significantly higher than that in their adjacent tissues, cirrhosis and normal liver tissues (all P<0.05), and its protein expression in tumor tissues was significantly higher than that in their adjacent tissues. The increased expression of caveolin-1 in HCC was associated with metastasis (P<0.05), and caveolin-1 expression was positively correlated with VEGF expression, MVD and UA (r=0.293, P=0.011; r=0.361, P=0.001; r=0.388, P=0.001). Conclusion: Increased caveolin-1 expression may promote the invasion and metastasis of HCC and the possible mechanism is that it induces VEGF expression in HCC and thereby enhances tumor angiogenesis.