烟草悬凝物诱导永生化人支气管上皮细胞恶性转化过程中p16基因甲基化改变的研究  

Study on p16 methylation status of BEP-2D cells during its malignant transformation by cigarette smoke condensate(CSC)

作　　者：张诚[1] 吴庆琛[1] 李强[1] 朱茂祥[2] 杨陟华[2] 潘秀颉[2] 谢俊豪[1] 

机构地区：[1]重庆医科大学附属第一医院胸心外科,重庆400016 [2]军事医学科学院放射与辐射医学研究所,北京100850

出　　处：《重庆医科大学学报》2008年第5期578-580,591,共4页Journal of Chongqing Medical University

摘　　要：目的:探讨永生化人支气管上皮细胞(HPV-18 immortalized human bronchial epithelial cells,BEP-2D)恶性转化过程中p16基因甲基化改变。方法:选取正常BEP-2D细胞及经过烟草悬凝物处理后的15周(week-15,W-15)、25周(W-25)、38周(W-38)和43周(W-43)的BEP-2D细胞作为研究对象,采用巢式MSP(Nested-methylation-specific PCR,Nested-MSP)检测各细胞株中p16基因的甲基化改变情况。结果:正常BEP-2D细胞p16基因未发生甲基化,而烟草悬凝物处理后的15周、25周、38周和43周的BEP-2D细胞p16基因发生甲基化。结论:p16基因甲基化改变可能发生在肺癌形成的早期,检测p16基因甲基化可以作为肺癌早期辅助诊断的生物标记物之一。Objective：To study p16 methylation of BEP-2D cells during its malignant transformation. Methods：Normal BEP-2D cells and BEP-2D cells treated by cigarette smoke condensate（CSC） for 15 weeks（W-15）,25 weeks（W-25）,38 weeks（W-38） and 43 weeks（W-43）respectively were chosen to study the p16 methylation status by Nested methylation specific PCR （Nested-MSP）. Results：The p16 methylation was found in W-15,W-25.W-38 and W-43 BEP-2D cells,but not in the normal BEP-2D cell. Conclusion-The p16 methylation may be considered as a kind of biology--marker of the early diagnosis of lung cancer because the p16 methylation occurs in the earlier period of lung cancer.

关 键 词：烟草悬凝物 P16 甲基化 巢式PCR 

分 类 号：R734.2[医药卫生—肿瘤]