目的 :研究特异性抗HPV16E6核酶对宫颈癌细胞恶性表型的影响。方法 :以脂质体法将抗HPV16E6核酶、空载体质粒分别导入CaSKi细胞 ,命名为CaSKi R ,CaSKi P细胞。测定CaSKi,CaSKi R ,CaSKi P 3种细胞的生长曲线和软琼脂克隆形成率 ,流式细胞仪检测 3种细胞中HPV16E6,PCNA ,C erbB 2蛋白的表达。将裸鼠分为 3组 ,分别在皮下接种CaSKi,CaSKi R ,CaSKi P细胞 ,检测细胞在裸鼠体内的成瘤能力 ;另取一组裸鼠 ,每只在右侧接种CaSKi细胞 ,左侧接种CaSKi R细胞 ,对比这两种细胞的致瘤性。分析特异性抗HPV16E6核酶对宫颈癌细胞恶性表型的影响。结果 :CaSKi P ,CaSKi细胞生长速率相近 ,CaSKi R细胞的生长速度明显降低。CaSKi R细胞的软琼脂克隆形成率明显低于CaSKi和CaSKi P细胞。与CaSKi细胞相比 ,CaSKi R细胞表达HPV16E6,PCNA ,C erbB 2蛋白明显减少 ,而CaSKi P细胞无此改变。CaSKi和CaSKi P在裸鼠体内的致瘤性无显著差异 ,而CaSKi R的成瘤性显著低于CaSKi。结论 :抗HPV16E6核酶的导入能部分逆转宫颈癌CaSKi细胞株的恶性表型 ,其原因可能在于病毒癌基因E6表达的降低 ,以及由此而引起的PCNA ,C erbB 2基因表达的降低 Objective: To investigate the effect of specific anti-HPV16E6 ribozyme on the malignant phenotype of cervical cancer cells. Methods: Anti-HPV16E6 ribozyme and empty vector plasmid were respectively introduced into CaSKi cells by liposome method and named CaSKi R and CaSKi P cells. The growth curves of CaSKi, CaSKi R and CaSKi P were measured and the rate of soft agar colony formation was determined. The expression of HPV16E6, PCNA and C erbB 2 in three kinds of cells was detected by flow cytometry. The nude mice were divided into 3 groups and inoculated subcutaneously with CaSKi, CaSKi R and CaSKi P cells respectively to detect the tumorigenic ability of the cells in nude mice. Another group of nude mice was inoculated with CaSKi cells on the right and left CaSKi R cells were seeded to compare the tumorigenicity of both cells. The effect of specific anti-HPV16E6 ribozyme on the malignant phenotype of cervical cancer cells was analyzed. Results: The growth rates of CaSKi P and CaSKi cells were similar, and the growth rate of CaSKi R cells was significantly decreased. The soft agar colony formation rate of CaSKi R cells was significantly lower than that of CaSKi and CaSKi P cells. Compared with CaSKi cells, CaSKi R cells expressed HPV16E6, PCNA and C erbB 2 protein decreased significantly, while CaSKi P cells did not change. The tumorigenicity of CaSKi and CaSKi P in nude mice was not significantly different, while that of CaSKi R was significantly lower than that of CaSKi. CONCLUSION: The introduction of anti-HPV16E6 ribozyme partially reverses the malignant phenotype of cervical cancer CaSKi cell line, which may be due to the decreased expression of viral oncogene E6 and the consequent reduction of PCNA and C erbB 2 gene expression