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环氧合酶-2 在肝细胞癌中的表达及其对肿瘤血管生成的影响[J]. 肿瘤防治研究, 2005, 32(04): 199-201. DOI: 10.3971/j.issn.1000-8578.696
引用本文: 环氧合酶-2 在肝细胞癌中的表达及其对肿瘤血管生成的影响[J]. 肿瘤防治研究, 2005, 32(04): 199-201. DOI: 10.3971/j.issn.1000-8578.696
Cyclooxygenase-2 Expression in Human Hepatocellular Carcinoma and Its Relationship with Angiogenesis[J]. Cancer Research on Prevention and Treatment, 2005, 32(04): 199-201. DOI: 10.3971/j.issn.1000-8578.696
Citation: Cyclooxygenase-2 Expression in Human Hepatocellular Carcinoma and Its Relationship with Angiogenesis[J]. Cancer Research on Prevention and Treatment, 2005, 32(04): 199-201. DOI: 10.3971/j.issn.1000-8578.696

环氧合酶-2 在肝细胞癌中的表达及其对肿瘤血管生成的影响

Cyclooxygenase-2 Expression in Human Hepatocellular Carcinoma and Its Relationship with Angiogenesis

  • 摘要: 目的 本研究通过检测肝细胞癌组织COX-2的表达,探讨COX-2与VEGF和MVD表达之间的关系,初步探讨COX-2在肝细胞癌血管生成的作用. 方法 应用免疫组化方法检测了45例肝细胞癌组织中COX-2和 VEGF、MVD的表达. 结果 肝癌、癌旁组织和正常肝组织中COX-2表达阳性率分别为73.3%、81.3%和100%.高分化癌组织中COX-2蛋白的表达显著高于中分化和低分化癌组织中的表达(P<0.05);癌组织中COX-2蛋白表达与年龄、性别、肿瘤大小、包膜、门静脉癌栓、AFP均无显著性差异(P>0.05).COX-2与VEGF表达和MVD有显著相关性(P<0.01,P<0.05). 结论 COX-2可通过增加VEGF的表达而促进肿瘤血管的生成.

     

    Abstract: Objective  This study was designed to investigate the expression and significance of COX-2 and the relationship between COX-2 and VEGF in hepatocellular carcinoma. Methods  The expression of COX-2 and VEGF were determined by immunohistochemical method in the samples of hepatocellular carcinoma. Results  The rate of positive expression COX-2 was 73. 3 %, 81. 3 % and 100 % in HCC tissues with adjacent nontumorous livers and normal hepatic tissue. The well differentiated HCC expressed that the COX-2 protein was st ronger than the moderate and poor differentiate HCC( P < 0. 05) . There was no significant relation-ship between the intensity of COX-2 expression and age, sex, tumor size, tumorcap-sule, presence of portal vein thrombosis and the level of fetoprotein ( P > 0. 05) . COX-2 express-ion was significantly correlated with VEGF expression ( P < 0. 01) and tumor MVD( P < 0. 05) in hepatocellular carcinoma. Conclusion  COX-2 may stimulate angiogenesis through VEGF upregulation.

     

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