EBV 诱导鼻咽上皮细胞逃避老化期过程中端粒酶活化和p16INK4A失活

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、p21^WAF1/CIPI和p53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p21^WAF1/CIPI和p53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p16^INK4A蛋白表达。

Telomerase activation and p16INK4a inhibition in the process of human nasopharyngeal epithelial cells escaping from replicative senescence induced by Epstein-Barr virus

Objective 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.