Carboxyl terminal activating region 3 of latent membrane protein 1 encoded by the Epstein-Barr virus regulates cell proliferation and protein expression in NP69 cells

In the present study, the mechanism by which carboxyl terminal activating region 3 (CTAR3) of latent membrane protein 1 (LMP1), encoded by the Epstein-Barr virus, regulated cell proliferation and protein expression was investigated in the nasopharyngeal epithelial cell line NP69. The deletion mutant LMP1 (LMP1(Δ232-351); amino acid residues including 232–351 codons in CTAR3 deleted) was generated by polymerase chain reaction. An NP69-LMP1(Δ232-351) cell line was established by retroviral infection. Finally, cell proliferation and protein expression of NP69 cells expressing LMP1(Δ232-351) were examined using a cell growth curve and western blot analysis. The results demonstrated: i) The proliferation of NP69-LMP1(Δ232-351) cells was significantly decreased compared with cells expressing wild type LMP1 (LMP1(WT); n=3; P<0.05); ii) 17 proteins exhibited differential protein expression (>2-fold change) in NP69-LMP1(Δ232-351) cells compared with NP69-LMP1(WT) cells; and iii) LMP1(WT) was involved in activating the Janus kinase 3 (JAK3) promoter and regulating the expression of JAK3 protein, while LMP1(Δ232-351) was almost defective in ability to activate the JAK promoter. These results suggested that LMP1-CTAR3 may be an important functional domain for regulating cell proliferation and protein expression in nasopharyngeal epithelial cells.