论文部分内容阅读
目的研究携带p53基因的新型增殖性腺病毒CNHK600-p53的导入是否增加肝癌细胞株PLC／PRF5对化疗药物的敏感性。方法采用四甲基偶氮唑盐(methylthiazolyl tetrazolium assay,MTT)法,观察化疗药物5-氟尿嘧啶(Fluorouracil,5-Fu)、丝裂霉素(Mitomycin,MMC)和表阿霉素(Epirubicin,EPI)单独及与CNHK600-p53联合对肝癌细胞株PLC／PRF5的杀伤效应。结果PLC／PRF5在5-Fu浓度为400μg／ml时细胞抑制率为(65±4．2)％,MMC浓度为1μg／ml细胞抑制率为(41±1．9)％,EPI浓度为10μg／ml细胞抑制率为(65±1．8)％。转入CNHK600-p53(MOI= 0．625)后再使用上述浓度的化疗药物,细胞抑制率分别为(89±5．3)％、(60±2．3)％和(75±1．5)％。当MOI值为0．3125,0．625,1．25时,CNHK600-p53组和Ad-p53组的细胞抑制率分别为(27±2．5)％、(30±3．7)％、(61±4．3)％和(4±2．7)％、(5±3．5)％、(16±4．5)％。结论单用CNHK600-p53效果优于Ad-p53,携带p53基因的CNHK600-p53能提高肝癌细胞株PLC／PRF5对化疗药物的敏感性。
Objective To investigate whether the introduction of a novel proliferating adenovirus CNHK600-p53 carrying the p53 gene increases the sensitivity of the hepatoma cell line PLC / PRF5 to chemotherapeutic drugs. Methods Methyl thiazolyl tetrazolium (MTT) method was used to observe the effects of chemotherapy drugs such as Fluorouracil (5-Fu), Mitomycin (MMC) and epirubicin ) Alone and in combination with CNHK600-p53 on hepatoma cell line PLC / PRF5 killing effect. Results The cell inhibition rate of PLC / PRF5 was (65 ± 4.2)% when the concentration of 5-Fu was 400μg / ml, (41 ± 1.9)% when the concentration of MMC was 1μg / ml and the concentration of EPI was 10μg / Ml cell inhibition rate was (65 ± 1.8)%. The results showed that the cell inhibitory rates were (89 ± 5.3)%, (60 ± 2.3)% and (75 ± 1.5)% respectively after transfection with CNHK600-p53 (MOI = 0.625) )%. The cell inhibitory rates of CNHK600-p53 group and Ad-p53 group were (27 ± 2.5)% and (30 ± 3.7)%, respectively, at MOI values of 0.3125, 0.625 and 1.25. (61 ± 4.3)% and (4 ± 2.7)%, (5 ± 3.5)% and (16 ± 4.5)%, respectively. CONCLUSION: CNHK600-p53 alone is superior to Ad-p53. CNHK600-p53 carrying p53 gene enhances the chemosensitivity of hepatoma cell line PLC / PRF5.