外源性P_(53)基因转染的人肝癌细胞化疗药物敏感性的研究  

Sensitivities of hepatoma cells transfected by exogenous P_(53) gene to chemotherapy

作　　者：杨晓红[1] 唐恩洁[1] 任碧轩[1] 

机构地区：[1]川北医学院免疫学与分子生物学研究室,四川南充637007

出　　处：《免疫学杂志》2005年第2期148-149,共2页Immunological Journal

基　　金：四川省教育厅和卫生厅重点课题资助 [川教计 (2 0 0 0 ) 2 5号 ;川卫科教发 (2 0 0 0 ) 3 4号 ]

摘　　要：目的　探讨外源性P53基因转染对人肝癌细胞系HepG 2化疗敏感性的影响。方法　将人野生型P53基因表达载体导入HepG 2细胞中,经筛选和鉴定后,采用MTT法观察其对甲氨蝶呤(MTX)和足叶乙甙(VP16 )作用后的HepG 2细胞生长抑制及凋亡的影响。结果　外源性P53基因在转染细胞中有效表达。增强了MTX和VP16对HepG 2细胞生长抑制并促进了药物诱导的细胞凋亡。结论　外源性P53基因能增加肝癌细胞对化疗药物的敏感性。Objective To investigate the effects of exogenous P 53 gene on chemosensitivity of huma hepatoma cell line. Methods The recombinant wild-type-PxT1-P 53 expression vector was constructed and the wild-type P 53 gene was transfected into human hepatoma cell line (HepG-2) with the calcium phosphase precipitation method. The effects of methotrexate (MTX) and etoposide (VP16) on the transfected cells were detected by assaying the rate of apoptosis and growth inhibition. Results The exogenous P 53 gene was expressed effectively in the cells, and the expression enhanced the apoptosis and growth inhibition of HepG-2 inducted by MTX and VP16. Conclusion The exogenous wild-type P 53 gene transfer can increase the drug sensibility of the hepatoma cells. The combination of P 53 gene therapy with chemotherapy may be more effective in cancer treatment.

关 键 词：野生型P53基因 人肝癌细胞系 化疗敏感性 

分 类 号：R735.7[医药卫生—肿瘤]