The activation of p53 mediated by Epstein-Barr virus latent membrane protein 1 in SV40 large T-antigen transformed cells.

摘要

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.