摘要
目的:探讨在体外培养的肺癌细胞A549中,AuroraA反义寡核苷酸对紫杉醇(PTX)化疗敏感性的影响,并分析其内在机制。方法:用脂质体瞬时转染法介导AuroraA反义硫代磷酸寡核苷酸(antisense oligodeoxyneucle-otides,ASODN)处理肺腺癌A549细胞6h后,给予一定浓度的PTX继续作用24h,用四唑氮蓝法(MTT)观察各组的量效反应,并计算半数抑制浓度IC50的值。Aurora A ASODN转染细胞后24及48h时应用流式细胞仪检测细胞周期分布的变化。结果:Aurora A ASODN作用于A549细胞后,细胞的生长抑制率呈剂量和时间依赖性,其中48h的IC50值约为300nmol/L;在此浓度和时间下,Aurora A反义寡核苷酸可使细胞周期阻滞于G2/M期。Aurora A ASODN转染增加了肺癌细胞A549对PTX的敏感性,ASODN+PTX组的细胞生长抑制率在30h达(70·51±1·77)%,明显高于单用ASODN的(29·98±2·05)%(P=0·000)和PTX的(33·61±1·57)%,P=0·000。结论:Aurora A ASODN增强肺腺癌细胞系A549对紫杉醇的化疗敏感性,这可能与Aurora A ASODN使细胞发生G2/M期阻滞有关。
OBJECTIVE,To study the effect of Aurora A antisense oligodeoxyneucleotides （ASODN） on chemosensitivity of paclitaxel （PTX） in lung cacer cell line A549 and discusse was its possible mechanisms. METHODS： PTX was given to each group after transfected with Aurora A ASODN for 6 hours, and reacted continually for another 24 hours, and the dose-effects response was observed by MTT assay and the value of IC50 was calculated in every group. Cell cycle distribution was observed by flow cytometry 24 hours and 48 hours after the transfection of Aurora A ASODN. RESULTS： The proliferation of the A549 cells transfected by lipofectamine 2 000 was inhibited by Aurora A ASODN in a dose and time dependent manner. It is also observed that the IC50 of A549 cells after 48 hour＇s treatment of ASODN was about 300 nmol/L. Besides, A549 cells showed an accumulation of cells in G2-M transition 24 h and 48 h after the transfection. Furhermore, the cell inhibition ratio of the combination of Aurora A ASODN and PTX [（70. 51±1.77）%] was higher significantly than that of paclitaxel [（33.61 ± 1.57）%] or Aurora A ASODN [（29. 98±2.05）%] alone, both P= 0. 000. CONCLUSION： Inhibition of Aurora A expression can results in the suppression of cell growth and chemosensitizing activity to PTX in human lung cancer cell line A549.
出处
《中华肿瘤防治杂志》
CAS
2007年第12期896-900,共5页
Chinese Journal of Cancer Prevention and Treatment
关键词
肺肿瘤
寡核苷酸类
反义
紫杉醇
lung neoplasms
antisense oligodeoxynucleotides
paclitaxel
