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目的:探讨羧基端截短的乙肝病毒x蛋白(Ct-HBx)和加帽蛋白B(CAPZB)在肝癌组织中的表达及临床意义。方法:应用PCR及测序技术检测41例HBsAg(+)的肝癌及癌周组织中HBx基因整合状态;采用免疫组化技术分别检测表达全长HBx和Ct-HBx的肝癌及癌周组织中CAPZB表达水平,分析CtHBx与CAPZB表达的关系,以及与临床病理特征之间的相关性。结果:(1)全长HBx基因在肝癌组织及癌周组织中表达率分别为20.6%(7/34)和40%(12/30),两者比较,差异无统计学意义(P=0.090);而3’末端缺失HBx基因在肝癌组织及癌周组织中表达率分别为79.4%(27/34)和53.3%(16/30),两者比较,差异有统计学意义(P=0.027)。(2)羧基端截短≥14个氨基酸(即碱基缺失≥42 bp)的标本有13例。对比全长HBx阳性的肝癌组织,CAPZB在Ct-HBx阳性肝癌组织中的表达明显减低;CAPZB在Ct-HBx阳性的肝癌及癌周组织中阳性表达率分别为23.1%(3/13)和84.6%(11/13),两者比较,差异有统计学意义(P=0.005)。CAPZB在肝癌组织中的表达水平与肝癌转移呈负相关关系(P=0.017)。结论:CAPZB在肝癌组织中的表达下调与HBx蛋白羧基端缺失突变有关,且与肝内转移发生相关,提示CAPZB可能参与了Ct-HBx介导的肝癌进展机制。
Objective: To investigate the expression and clinical significance of Ct-HBx and CAPZB in hepatocellular carcinoma (HCC). Methods: The integrated status of HBx gene in 41 cases of HBsAg (+) and pericarcinoma tissues was detected by PCR and sequencing. The expression of CAPZB in hepatocellular carcinoma and peri-cancerous tissues was detected by immunohistochemistry Level, analyze the relationship between CtHBx and CAPZB expression, and the correlation with clinicopathological features. Results: (1) The expression of full length HBx gene was 20.6% (7/34) and 40% (12/30) in hepatocellular carcinoma and pericarcinoma tissues, respectively, with no significant difference (P = 0.090 ), While the expression of HBx gene at the 3’-end was 79.4% (27/34) and 53.3% (16/30) respectively in hepatocellular carcinoma and pericarcinoma tissues, the difference was statistically significant (P = 0.027 ). (2) Thirteen cases were detected with truncated carboxyl terminal> 14 amino acids (ie base deletion> = 42 bp). Compared with full-length HBx-positive hepatocarcinoma, the expression of CAPZB in Ct-HBx positive hepatocellular carcinoma was significantly reduced. The positive expression rate of CAPZB in Ct-HBx positive hepatocellular carcinoma and pericarcinoma tissues was 23.1% (3/13) and 84.6 % (11/13), the difference between the two was statistically significant (P = 0.005). The expression of CAPZB in HCC was negatively correlated with the metastasis of HCC (P = 0.017). CONCLUSIONS: The down-regulation of CAPZB expression in HCC tissues is related to the deletion of the carboxyl terminal of HBx protein and is associated with intrahepatic metastasis, suggesting that CAPZB may be involved in the mechanism of Ct-HBx-mediated liver cancer progression.