重组腺病毒介导CD自杀基因联合野生型p53基因对直肠癌细胞的杀伤作用  被引量:4

Antitumor effects of coinfection of CD suicide gene and wild type p53 gene with adenovirus mediation on rectal cancer cells

在线阅读下载全文

作  者:于波[1] 李世拥[1] 安萍[1] 陈钢[1] 蔡惠云[1] 郭文华[1] 

机构地区:[1]北京军区总医院普外科,10070

出  处:《中华实验外科杂志》2001年第1期25-26,共2页Chinese Journal of Experimental Surgery

基  金:国家自然科学基金资助项目 !(39870 737)

摘  要:目的 观察重组腺病毒介导胞嘧啶脱氨酶 (CD)基因和人野生型 p5 3基因共转染对直肠癌细胞的杀伤作用。方法 用携带CD/p5 3、CD、p5 3基因腺病毒感染直肠癌细胞SW 837,计数瘤细胞集落数 ,采用四唑蓝比色 (MTT法 )检测瘤细胞存活率。于 6 0只裸鼠移植瘤内注射重组腺病毒、磷酸盐缓冲液 (PBS) ,测定肿瘤生长抑制率。结果 用CD/p5 3、CD、p5 3重组腺病毒感染SW 837细胞 ,加 5 FC后细胞集落形成分别为 :6、38、6 9。裸鼠移植肿瘤生长抑制率分别为 78.6 %、5 6 .5 %、2 2 .3 %。CD/p5 3重组腺病毒感染组肿瘤细胞集落形成和存活率下降最显著 (P <0 .0 1) ,对肿瘤的抑制作用最明显。结论 CD自杀基因与野生型p5Objective To investigate antitumor effects of cytosine deaminase (CD) suicide gene/5 fluorocytosine (5 FC) and human wild type p53 gene with adenovirus mediation on rectal cancer cells. Methods With adenovirus carrying CD/p53, CD, p53 genes, SW837 rectal cancer cells were infected, and plating efficiency was counted. Surval rate of the tumor cells was tested with MTT method. The recombinant adenovirus were injected into xenograft tumors of SW837 cells in 60 nude mice. Suppression rate of tumor growth was examined. Results Plating efficiency of the SW837 cells infected by recombinant adenovirus with CD/p53, CD, p53 genes, adding 5 FC in each group, was 6, 38, 69 respectively. Suppression rate of tumor growth was 78.6%, 56.5%, 22.3% in ilka group. The decreases of plating efficiency and surval rate of tumor cells in CD/p53 recombinant adenovirus infection group were the most significant ( P <0.01 ). And a strong suppression of xenograft tumor was observed by combination of CD/5 FC with wild type p53. Conclution Coinfection of CD and wild type p53 genes has more powerful antitumor actions.

关 键 词:直肠肿瘤 基因治疗 p53基因 重组腺病毒 CD自杀基因 

分 类 号:R735.37[医药卫生—肿瘤] R730.5[医药卫生—临床医学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象