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The activation of p53 mediated by Epstein‐Barr virus latent membrane protein 1 in SV40 large T‐antigen transformed cells
Author(s) -
Li Lili,
Zhou Shanghui,
Chen Xue,
Guo Lili,
Li Zijian,
Hu Duosha,
Luo Xiangjian,
Ma Xiaoqian,
Tang Min,
Yi Wei,
Tsao Sai Wah,
Cao Ya
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.01.031
Subject(s) - nasopharyngeal carcinoma , carcinogenesis , epstein–barr virus , virus , biology , antigen , cancer research , gene , tumor suppressor gene , virology , microbiology and biotechnology , immunology , genetics , medicine , radiation therapy
The Epstein‐Barr virus (EBV) encoded latent membrane protein 1 (LMP1) plays an important role in the carcinogenesis of nasopharyngeal carcinoma (NPC). The tumor suppressor p53 is an important transcription factor. The mutation of the p53 gene is the frequent alteration in most of tumors, but nearly 100% wild‐type p53 gene is found in NPC biopsy. Here, our study testified that SV40 T‐antigen transformed nasopharyngeal epithelial cells contained free, wild‐type p53. Moreover, LMP1 regulated p53 both at transcriptional and translational level. Furthermore, the mechanism of p53 accumulation mediated by LMP1 from post‐translational level‐phosphorylation and ubiquitination were determined. Therefore, the effects of EBV LMP1 on p53 may potentially contribute to EBV‐associated pathogenesis.