肝细胞癌组织及卵圆细胞中细胞角质素18及消减基因P02的表达

Expressions of CK18 and subtractive gene P02 in hepatocellular carcinoma tissue and oval cells

目的:观察肝细胞癌、癌周肝硬化组织及卵圆细胞中细胞角质素18(CK18)及消减基因P02的表达情况。方法:采用免疫组化SP法观察8例正常肝组织,27例肝硬化组织和43例肝细胞癌组织中CK18的表达;采用原位杂交方法检测肝细胞癌、癌周肝硬化组织及卵圆细胞中P02的表达。结果:肝硬化组织和正常肝组织中CK18阳性表达率分别为29.6%和25.0%(P>0.05),肝细胞癌组织中CK18阳性表达率为65.1%,与肝硬化组和正常肝组织比较差异有统计学意义(P<0.05)。在13对肝硬化的汇管区和肝细胞癌癌巢周边可见到卵圆细胞中P02的强阳性表达,且其数量在2种组织中差异有统计学意义(P<0.05)。结论:CK18参与了肝硬化到肝细胞癌的癌变过程;CK18在卵圆细胞中的强阳性表达,及其在肝细胞癌和肝硬化组织中数量上的显著性差异,证明卵圆细胞与肝脏损伤后再生及癌变有关,支持肝细胞癌的卵圆细胞起源学说;P02是一个肝细胞癌高表达基因,可能通过促进卵圆细胞的增殖来介导肝细胞癌的发生。

Aim： To observe the expression of cytoketatinl8 and subtractive gene P02 in hepatocellular carcinoma, cirrhosis of liver, and oval cell. Methods：Immunohistochemical streptavidin-peroxidase （SP） method was adopted to examine the expressions of cytoketatinl8 in 8 cases of normal liver, 27 cases of cirrhosis, and 43 cases of hepatocellular carcinoma samples. DIG-probe Synthesis kit was adopted to prepare for P02 probe by PCR and in situ hybridization was used to detect the expression of subtractive gene P02 in 15 pairs of hepatocellular carcinoma, cirrhosis of liver, and oval cell. Results： The positive rate of eytoketatinl8 in cirrhosis of liver, normal liver and hepatoeellular carcinoma were 29.6% , 25.0% , and 65.1% , and there were significant differences between hepatoeellular carcinoma and cirrhosis of liver, normal liver （P 〈 0.05 ）. Oval cells with P02 strong positive staining could be seen in the portal area of cirrhosis and in the brink of carcinoma, and there were significant differences in the numbers of them in cirrhosis of liver and hepatocellular carclnoma（P 〈 0.05 ）. Conclusion： cytoketatinl8 is involved in the carcinogenesis of hepatocellular carcinoma. Oval cells are strongly positive for cytoketatinl8 in cirrhosis of liver and hepatoeellular carcinoma. Oval cells are connected with regenera- tion of liver, and is probably the original cell of hepatocellular carcinoma. P02 is overexpressed in hepatoeellular carcinoma, which may play an important role during carcinogenesis of hepatocellular carcinoma by promoting the proliferation of oval cells.