Epstein-Barr virus inhibits P16INK4a expression in human fetal nasopharyngeal epithelial cells escaping from the replicative senenscence

Jing Yang, Lin Deng, Xin Song, Lin Ding, Xi Yun Deng, Wei Yi, Y. Cao

Research output: Contribution to journalArticle

3 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)215-220
Number of pages6
JournalShi yan sheng wu xue bao
Volume36
Issue number3
StatePublished - Jun 2003
Externally publishedYes

ASJC Scopus subject areas

  • Medicine(all)

Fingerprint Dive into the research topics of 'Epstein-Barr virus inhibits P16INK4a expression in human fetal nasopharyngeal epithelial cells escaping from the replicative senenscence'. Together they form a unique fingerprint.

Cite this