5-脱氧氮杂胞苷上调肺癌细胞p16_(INK4A)基因表达的作用观察  

Observation on the Role of 5-Aza-2`-Deoxycytidine Up-regulating p16_(INK4A)Gene Expression

作　　者：白明[1] 张晓菊[1] 金阳[1] 陶晓南[1] 

机构地区：[1]华中科技大学同济医学院附属协和医院呼吸内科,武汉430022

出　　处：《同济医科大学学报》2001年第3期289-291,共3页Acta Universitatis Medicinae Tongji

基　　金：湖北省自然科学基金资助项目 (98J10 2 )

摘　　要：肺癌细胞 SPC- A1经 5 -脱氧氮杂胞苷 (5 - Aza- cd R)处理后 ,应用逆转录聚合酶链反应 (RT- PCR)及免疫细胞化学检测其在 m RNA和蛋白质水平的变化 ,同时 MTT法观察肺癌细胞 SPC- A1增殖能力的改变。结果表明经 5 -Aza- cd R处理后 ,肺癌细胞 SPC- A1中 p16 INK4A基因的 m RNA及蛋白质表达都有所上调 ,MTT法亦显示处理后的 SPC-A1细胞增殖速率减缓。说明 5 - Aza- cd R通过对 p16 INK4A基因 5 ` CPG岛的去甲基化作用 ,上调 p16 INK4A基因的 m RNA转录及蛋白表达 。The alterations of expression of p16 INK4A mRNA and protein were inspected by using RT PCR and immunocytochemistry staining methods after the lung cancer cells SPC A1 were treated with 5 Aza 2′ deoxy cytidine (5 Aza cdR). Meanwhile,MTT assay was used to observe the change of the proliferation activity of lung cancer cells SPC A1 before and after treated with 5 Aza cdR). The results showed that the expression of p16 INK4A mRNA and protein was up regulated in SPC A1 after treated with 5 Aza cdR. MTT assay also showed the proliferation activity of SPC A1 treated with 5 Aza cdR was obviously reduced. The results suggest that 5 Aza cdR may up regulate the expression of p16 INK4A mRNA and protein by de novo methyation, so this can restore its function of suppressing the proliferation of lung cancer cell.

关 键 词：5-脱氧氮杂胞苷 肺癌 p16NK4A基因 甲基化 

分 类 号：R734.2[医药卫生—肿瘤]