title: [Epstein-Barr virus inhibits P16INK4a expression in human fetal nasopharyngeal epithelial cells escaping from the replicative senenscence].
abstract: Cell cycle deregulation is regarded as an important event to involve in cellular immortalization. To confirm the role of cell cycle deregulation in human fetal nasopharyngeal epithelial cells escaping from the replicative senescence induced by Epstein-Barr virus infection, we detected expression of cell cycle regulators, such as p16INK4a, p21WAF1/CIP1, p53, and E2F1 with Western blotting and immunocytochemisty in this study. Our results found that Epstein-Barr virus inhibited the expression of p16INK4a, at the same time, E2F1 expression were strongly increased in EBV-infected cells, however, as for the expression of p53 and p21WAF1/CIP1, there was no difference between EBV-infected cells and non-infected cells. The results show that EBV inactivates p16INK4a/pRB pathway and then induces E2F1 activity and it is implicated that Epstein-Barr virus-medicated cell cycle deregulation plays an important role in the immortalization of human nasopharyngeal epithelial cells. These data will be helpful for further studying the carcinogenesis of nasopharyngeal carcinoma.
authors.affiliation: Cancer Research Institute, Xiangya Medical School, Central South University, Changsha, Hunan 410078, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Yang
authors.forename: Lin
authors.initials: L
authors.lastname: Deng
authors.forename: Xin
authors.initials: X
authors.lastname: Song
authors.forename: Lin
authors.initials: L
authors.lastname: Ding
authors.forename: Xi Yun
authors.initials: XY
authors.lastname: Deng
authors.forename: Wei
authors.initials: W
authors.lastname: Yi
authors.forename: Ya
authors.initials: Y
authors.lastname: Cao
mesh_terms: D002471:Cell Transformation, Neoplastic; D016922:Cellular Senescence / Q000235:genetics*; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000096:biosynthesis* / Q000235:genetics; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins / Q000096:biosynthesis / Q000235:genetics; D004847:Epithelial Cells / Q000473:pathology / Q000821:virology; D005333:Fetus; D004854:Herpesvirus 4, Human / Q000235:genetics*; D006801:Humans; D009303:Nasopharyngeal Neoplasms / Q000821:virology; D009305:Nasopharynx / Q000473:pathology / Q000821:virology*; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis / Q000235:genetics
chemical_list: C493956:CDKN1A protein, human; D019941:Cyclin-Dependent Kinase Inhibitor p16; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins; D016159:Tumor Suppressor Protein p53