研究类泛素化蛋白酶-1（sentrin-specific protease-1，SENP-1）基因在不同侵袭潜能肝细胞肝癌细胞株及人永生化肝细胞中mRNA和蛋白的表达水平及其与肝癌细胞侵袭能力的关系。方法：使用RT-PCR、Real-time PCR、Western blotting和免疫荧光方法对肝癌细胞株MHCC97L（低侵袭性）、MHCC97H和HCCLM3（高侵袭性）、SMMC-7721和HepG2（无明显侵袭性）SENP-1 mRNA和蛋白表达水平进行检测，以人永生化肝细胞株HL-7702为对照，分析SENP-1的表达与肝癌细胞株侵袭转移能力的关系。结果：RT-PCR和Real-time PCR检测结果显示，SENP-1 mRNA（F=5.658；P=0.042）和蛋白（F=88909，P=0.000）在肝癌细胞株中的表达随着肝癌细胞株侵袭潜能的增高而增高；Western blotting检测结果显示，5种肝癌细胞株SENP-1蛋白水平均显著高于人永生化肝细胞株；免疫荧光法观察发现，SENP-1蛋白在肝癌细胞株内主要为胞质表达，部分胞核表达。结论：SENP-1基因在肝癌细胞株中的高表达可能具有促进肝癌细胞侵袭转移的作用。

To determine mRNA and protein levels of sentrin-specific protease 1 (SENP-1) in human non-tumor hepatic cells and various types of human hepatocellular carcinoma (HCC) cells with different invasive and metastatic capacities. Methods: Low invasive HCC cell lines MHCC97L, high invasive HCC cell lines MHCC97H and HCCLM3, non-invasive HCC cell lines SMMC-7721and HepG2 and immortalized normal liver cell line HL-7702 were utilized. Their levels of SENP-1 mRNA and protein were determined by RT-PCR andquantitative real-time PCR and Western blotting respectively while the intracellular location of SENP-1 assessed by immunofluorescence staining. Results: RT-PCR and real-time PCR analyses showed that SENP-1 mRNA abundance was significantly different between the cell lines evaluated (F=5.658；P=0.042) and increased with the incisive capacity of the cells. protein (F=88.909, P=0.000) in HCC cell lines were increased significantly. Western blotting analysis showed that SENP-1 protein levels were significantly higher in all five HCC cell lines tested as compared the immortalized normal liver cell line (F=88.9, P=0.0001). Immumofluorescence staining revealed that SENP1 protein was localized predominantly in cytolymph and in a small quantity in the nucleus. Conclusion: The higher the invasive and metastatic capacities of hepatocellular carcinoma cells, the higher the SENP-1 mRNA and protein levels. This observation suggests that SENP-1 may promote hepatocellular carcinoma cell invasion and metastasis．

广州市白云区科技计划项目资助（No.2011-KZ-56）