中文摘要：

目的探讨有慢性HBV感染史的原发性肝癌患者癌组织与癌旁组织驱动蛋白家族成员4A（KIF4A）表达的差异，了解HBV对KIF4A表达的影响。方法采用RT—PCR和Western印迹法检测患者癌组织和癌旁组织KIF4A的表达；将浓度分别0、0．2、0．4、0．6和0．8μg／mL的HBV感染性克隆pHBV1．3与KIF4A基因启动子共转染HepG2细胞，并测定荧光素酶的活性；检测HepG2细胞转染pHBV1．3后KIF4AmRNA和蛋白表达变化；统计学分析采用t检验。结果KIF4A在癌组织表达显著高于癌旁组织，HBV能激活KIF4A基因启动子的活性，且随着pHBV1．3浓度的增加，荧光素酶活性也不断增强，分别为（126．8土13．4）、（219．8±16．7）、（387．6±21．5）、（586．5±228．9）和（657．6±35．5）RUL／／ag蛋白，转染不同剂量的空白对照组，荧光素酶活性分别为（123．6±13．8）、（131．8±14．6）、（129．7±13．5）、（135．3±13．4）和（127．1±12．7）RUL／μg蛋白，两组比较，差异有统计学意义（t=4．875，P=0．006）；HBV在mRNA和蛋白水平上调KIF4A的表达，且这种激活作用随着pHBV1．3浓度的增加而增强。结论原发性肝癌患者KIF4A表达水平升高，HBV能上调KIF4A的表达。

英文摘要：

Objective To investigate the differences of kinesin family member 4 （KIF4A） expression between hepatic carcinoma and adjacent tissue in patients with chronic hepatitis B virus （HBV） infection, and to understand the effect of HBV on the expression of K1F4A. Methods Reverse transcriptase-polymerase chain reaction and Western blot were used to measure the expression of KIF4A in hepatic carcinoma and adjacent tissues. HepG2 cells were co-transfected with KIF4A promoter containing the luciferase gene and HBV infectious clone pHBV1. 3, and luciferase activity was measured. Expression of KIF4A in HepG2 cells was measured after tranfected with different doses of pHBV1.3. The student＇s t-test was used for statistic analysis. Results Expression of KIF4A was much higher in hepatic carcinoma than that in adjacent tissues. HBV enhanced KIF4A gene promoter activity and the luciferase activities were increased as the concentration of pHBV1. 3 increased （0, 0.2, 0.4, 0.6 and 0. 8 /,g/mL）, which were （126. 8±13. 4）, （219. 8±16. 7）, （387. 6± 21.5）, （586.5±28.9） and （657. 6±35. 5） RUL/μg protein, respectively, while thelueiferase activities were （123.6±13.8）, （131.8±14.6）, （129.7±13.5）, （135.3±13.4） and （127.1±12.7） RUL/μg protein, respectively with different doses of control plasmids transfected, and statistical analysis showed significant difference between them （t= 4.875, P= 0. 006）. And HBV upregulated KIF4A mRNA and protein expressions in HepG2 cells in a concentration-dependent manner. Conclusion Expression of KIF4A is enhanced in hepatic carcinoma and HBV can upregulate KIF4A expression.