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目的探讨血管内皮生长因子(VEGF)和促血管生成素(Angiopietin)及其受体Tie2在启动肝细胞癌(HCC)血管生成中的调控机制及在HCC发生发展中的作用。方法新鲜HCC标本及癌旁肝组织38例,用实时定量逆转录-聚合酶链反应(RT-PCR)的方法检测Ang-1、Ang-2、Tie2和VEGF在各组织标本中的表达,以CD34标记新生血管内皮并计数微血管密度(MVD),分析上述因子在HCC组织和非癌肝组织中的表达差异、相互作用及其与MVD、临床病理特征之间的关系。结果Ang-1、Tie2在HCC和非癌肝组织中的表达差异无统计学意义(0．194 7±0．086 2比0．232 6±0．109 8,1．601 6±0．900 7比1．340 0±0．703 7,P均>0．05),而VEGF和Ang-2在HCC组织的表达高于非癌肝组织(1．038 0±0．572 0比0.832 3±0．182 4,0．621 3±0.417 6比0．442 9±0．330 1,P均<0．05);VEGF、Ang-2、Ang-2／1都与MVD和临床病理特征相关(P<0．01),但与组织分化程度无关(P>0．05)。结论Ang-2／1的失衡表达及其与VEGF和Tie2的共同作用是启动肝组织血管生成并诱发HCC发生、发展的重要因素;这种因素在HCC中的持续作用进一步促进了肿瘤血管生成和恶性生物学行为。
Objective To investigate the regulatory mechanism of vascular endothelial growth factor (VEGF), angiopoietin (Angiopietin) and its receptor Tie2 in the initiation of hepatocellular carcinoma (HCC) angiogenesis and its role in the development of HCC. Methods The fresh HCC specimens and the adjacent liver tissues of 38 cases were used to detect the expression of Ang-1, Ang-2, Tie2 and VEGF in tissue samples by real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR). Endothelial neovascularization was marked by CD34 and the microvessel density (MVD) was counted. The expression and interaction of these factors in HCC tissue and non-cancerous liver tissue were analyzed and their relationship with MVD and clinicopathological features were analyzed. Results There was no significant difference in the expression of Ang-1 and Tie2 in HCC and non-cancerous liver tissue (0.194 7±0.086 2 vs 0.232 6±0.109 8, 1.601 6±0.900 7 compared to 1.340 0±0.703 7, all P>0.05), while the expression of VEGF and Ang-2 in HCC tissue was higher than that in non-cancerous liver tissue (1.038 0±0.572 0 vs. 0.832 3 ± 0.182 4, 0.621 3 ± 0.417 6 vs. 0.442 9 ± 0.330 1, P <0.05); VEGF, Ang-2, Ang-2/1 all with MVD and clinicopathological features Correlation (P<0.01), but not related to tissue differentiation (P>0.05). Conclusion The unbalanced expression of Ang-2/1 and its co-action with VEGF and Tie2 are important factors that trigger hepatic angiogenesis and induce the development and progression of HCC. The sustained effect of this factor in HCC further promotes tumor angiogenesis and Malignant biological behavior.