Although previous studies showed that the principal oncoprotein encoded by Epstein-Barr virus, latent membrane protein 1 (LMP1), could induce the nasopharyngeal carcinoma cells in G2/M phase increased, littleis known ...Although previous studies showed that the principal oncoprotein encoded by Epstein-Barr virus, latent membrane protein 1 (LMP1), could induce the nasopharyngeal carcinoma cells in G2/M phase increased, littleis known about the target molecules and mechanisms. The present study demonstrated that LMP1 couldinduce the accumulation of p53 protein and upregulate its transactivity in a dose dependent manner, whichresulted in the decrease of the kinase activity of cdc2/cyclin B complex and inducing arrest at G2/M phasethrough the activation of NF-kB and AP-1 signaling pathways, and the effect of NF-kB was more obviousthan that of AP-1. This study provided some significant evidence for further elucidating the molecular mechanisms that LMP1 had effects on the surveillance mechanism of cell cycle and promoting the survivalof transformed cells and tumorigenesis.展开更多
文摘Although previous studies showed that the principal oncoprotein encoded by Epstein-Barr virus, latent membrane protein 1 (LMP1), could induce the nasopharyngeal carcinoma cells in G2/M phase increased, littleis known about the target molecules and mechanisms. The present study demonstrated that LMP1 couldinduce the accumulation of p53 protein and upregulate its transactivity in a dose dependent manner, whichresulted in the decrease of the kinase activity of cdc2/cyclin B complex and inducing arrest at G2/M phasethrough the activation of NF-kB and AP-1 signaling pathways, and the effect of NF-kB was more obviousthan that of AP-1. This study provided some significant evidence for further elucidating the molecular mechanisms that LMP1 had effects on the surveillance mechanism of cell cycle and promoting the survivalof transformed cells and tumorigenesis.
