Abstract
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.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Antigens, Viral, Tumor / genetics
-
Antigens, Viral, Tumor / metabolism*
-
Cell Extracts
-
Cell Line, Transformed
-
Epithelial Cells / cytology
-
Epithelial Cells / metabolism
-
Epithelial Cells / radiation effects
-
Gene Expression Regulation / radiation effects
-
Humans
-
Immunoprecipitation
-
Nasopharynx / cytology
-
Nasopharynx / metabolism
-
Nasopharynx / radiation effects
-
Protein Biosynthesis / radiation effects
-
Protein Transport / radiation effects
-
RNA, Messenger / genetics
-
RNA, Messenger / metabolism
-
Radiation, Ionizing
-
Simian virus 40*
-
Transcription, Genetic / radiation effects
-
Tumor Suppressor Protein p53 / genetics*
-
Tumor Suppressor Protein p53 / metabolism*
-
Ubiquitination / radiation effects
-
Viral Matrix Proteins / metabolism*
Substances
-
Antigens, Viral, Tumor
-
Cell Extracts
-
EBV-associated membrane antigen, Epstein-Barr virus
-
RNA, Messenger
-
Tumor Suppressor Protein p53
-
Viral Matrix Proteins