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目的探讨DKK-3和WIF-1基因启动子甲基化状态与肝细胞癌发生的相关性。方法应用甲基化特异性聚合酶链反应检测33例肝细胞癌及相应的癌旁组织和20例正常对照肝组织中DKK-3和WIF-1基因启动子甲基化状态,分析上述组织中两种基因甲基化状态与临床资料的关系。结果DKK-3和WIF-1基因在癌组织中甲基化率明显高于癌旁组织和正常组织(P<0.05,P<0.05),而癌旁组织和正常组织中DKK-3和WIF-1基因甲基化率相比无明显差异;癌组织中DKK-3基因甲基化与临床资料中年龄及肝硬化有关;癌组织中WIF-1基因甲基化与临床资料中乙肝表面抗原、肝硬化有关。结论DKK-3和WIF-1基因启动子甲基化与HCC的发生相关;DKK-3和WIF-1基因致肝细胞癌的发生机制可能与肝硬化致肝细胞癌的发生机制不尽相同,两者是否有相互作用尚不清楚。
Objective To investigate the relationship between the methylation status of DKK-3 and WIF-1 promoter and the occurrence of hepatocellular carcinoma. Methods The methylation status of promoter of DKK-3 and WIF-1 gene in 33 hepatocellular carcinoma and its corresponding paracancerous tissues and 20 normal control liver tissues was detected by methylation-specific polymerase chain reaction Relationship between Methylation Status of Two Genes and Clinical Data. Results The methylation rates of DKK-3 and WIF-1 in cancer tissues were significantly higher than those in paracancer tissues and normal tissues (P <0.05, P <0.05), but DKK-3 and WIF- 1 gene methylation rate compared with no significant difference; DKK-3 gene methylation in cancer tissue and clinical data age and cirrhosis; WIF-1 gene methylation in cancer and clinical data of hepatitis B surface antigen, Cirrhosis related. Conclusions The promoter methylation of DKK-3 and WIF-1 genes is related to the occurrence of HCC. The mechanism of carcinogenesis of hepatocellular carcinoma induced by DKK-3 and WIF-1 genes may be different from that of hepatocellular carcinoma. Whether the interaction between the two is unclear.