野生型P53、P16基因协同对肺腺癌细胞系生长抑制作用的研究  

Expression of Wild-type P53 Gene and P16 Gene in Lung Adenocarcinoma Cell Lines

作　　者：闫承慧[1] 王柏秋[1] 吴焱[1] 傅松滨[1] 李璞[1] 

机构地区：[1]哈尔滨医科大学医学遗传学研究室,黑龙江哈尔滨150086

出　　处：《遗传》2001年第1期1-4,共4页Hereditas（Beijing)

基　　金：黑龙江省科学技术计划攻关和青年科学基金!资助项目 (Q98 9);黑龙江省科学技术计划攻关项目! (G99C2 0 6 1)资助

摘　　要：为了探讨野生型P5 3基因及P16基因在恶性肿瘤基因治疗中的作用 ,用腺病毒为载体将野生型P5 3基因转入高、低转移的肺腺癌细胞系Anip973、AGZY83 -a和经野生型P16基因质粒转染的高、低转移肺腺癌细胞系Anip973(Anip973P16 )、AGZY83-a(AGZY83-aP16 )。对各组转染细胞进行生长曲线、MTT生长抑制率、原位末端标记、Western -blotting等技术检测分析。结果发现 (1)野生型P5 3蛋白的过表达对上述肺腺癌细胞系均呈现出较强的生长抑制作用。 (2 )野生型P5 3蛋白的过表达对高转移肺癌细胞系Anip973的抑制作用明显高于低转移细胞系AGZY83 -a。 (3)野生型p5 3蛋白的过表达对经野生型P16基因转染的高、低转移的肺癌细胞Anip973、AGZY83-a抑制作用明显高于未经P16基因转染的细胞。野生型P5 3基因可以作为肺腺癌基因治疗的候选基因。肿瘤抑制基因P5 3、P16的联合转染可能是对肺腺癌进行基因治疗的有效手段。To investigate the suppression effect of tumor suppressor genes in lung adenocarcinoma cell lines,we transferred a pair of lung adenocarcinoma cell lines with different metastasis potential,Anip973(High metastasis potential cell line) and AGZY83-a (Low metastasis potential cell line)and this pair of cell lines transfected with P16 gene:AGZY83-a P16 and Anip973 P16 with wild type P53 gene with adenovirus vector.The suppression effects of P53 gene were evaluated by cell growth curve,MTT,western blotting analysis and TUNEL technique.Overexpression of wild type P53 gene in AGZY83-a,Anip973,Anip973 P16 and AGZY83-a P16 inhibited the growth of these four kinds of lung cancer cells and induced apoptosis of the cells.The suppression effect of P53 gene in Anip973 and Anip973 P16 was higher than AGZY83-a and AGZY83-a P16 while co expression of P53 and P16 in this pair of cell lines inhibited the cells more efficiently comparing with the expression of P53 alone.Wild type P53 gene might act as a candidate gene in lung adenocarcinoma gene therapy while co transfection of P53 and P16 genes was a more effective method.

关 键 词：野生型P53基因 P16基因 腺病毒 高转移肺癌细胞系 ANIP973 低转移肺癌细胞系AGZY83-a 

分 类 号：R734.2[医药卫生—肿瘤]