EBV诱导鼻咽上皮细胞逃避老化期过程中端粒酶活化和p16^(INK4A)失活  

Telomerase activation and p16^(INK4a) inhibition in the process of human nasopharyngeal epithelial cells escaping from replicative senescence induced by Epstein-Barr virus

作　　者：杨静[1] 邓琳[2] 丁琳[2] 邓锡云[2] 宋鑫[2] 曹亚[2] 

机构地区：[1]广州医学院实验医学研究中心,广州510182 [2]中南大学湘雅医学院肿瘤研究所,长沙410078

出　　处：《现代肿瘤医学》2003年第2期87-90,共4页Journal of Modern Oncology

基　　金：国家重点基础研究发展规划 (973) (G19980 5 12 0 1);国家自然科学基金(30 2 0 0 32 8)

摘　　要：目的　探讨EB病毒诱导人鼻咽上皮细胞逃避老化期的分子机制。方法　SA - β -Gal染色法观察人鼻咽上皮细胞逃避老化期 ;PCR -银染法、S -P免疫组化法分别检测端粒酶活性和 p16 INK4A、p2 1WAF1/CIP1和 p5 3的表达情况。 结果　EB病毒感染组细胞表达SA - β Gal活性下降 ,并表达端粒酶活性 ,而 p16 INK4A蛋白不表达 ,但 p2 1WAF1/CIP1和 p5 3蛋白表达无明显变化。 结论　人鼻咽上皮细胞逃避老化期过程中EB病毒激活端粒酶和抑制 p16Objective To study the mechanism that the Eptein-Barr virus induces human nasopharyngeal epithelial cells escaping from thereplicative senescence.Methods The senescence-associated beta-galactosidase(SA-beta-Gal)staining was used to observe the escaping from replicative senescence,the PCR-Ag NO3 assay (Roche Diagnostics GmbH,Mannheim,Germany),and S-P immunocytochemical assay were adopted for detecting telomerase activity and the expression of p16 CIP1/WAF1 and p53.Results A low percentage of EBV-infected cells was found to express SA-beta-Gal activity.The results suggested that EBVwas capable of suppressing the replicative senescence of human nasopharyngeal epithelial cells.Furthermore,telomerase activity was found in EBV-infected cells.And also,p16 INK4a was detected to expressin EBV-infected cells but not in non-infected cells.However,the expression of p21 CIP1/WAF1 and p53 were not apparently different between EBV-infected cells and non-infected cells. Conclusion It is suggested that EBV ectivates ES telomerase and inhibits p16 INK4a expression in the process ofhuman nasopharyngeal epithelial cells escaping from the replicative senescence.

关 键 词：老化期 端粒酶活性 p16^INK4A失活 EB病毒 人鼻咽上皮细胞 鼻咽癌 

分 类 号：R739.62[医药卫生—肿瘤] R739.63[医药卫生—临床医学]