Abstract
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 (LMP1Δ232‑351; amino acid residues including 232‑351 codons in CTAR3 deleted) was generated by polymerase chain reaction. An NP69‑LMP1Δ232‑351 cell line was established by retroviral infection. Finally, cell proliferation and protein expression of NP69 cells expressing LMP1Δ232‑351 were examined using a cell growth curve and western blot analysis. The results demonstrated: i) The proliferation of NP69‑LMP1Δ232‑351 cells was significantly decreased compared with cells expressing wild type LMP1 (LMP1WT; n=3; P<0.05); ii) 17 proteins exhibited differential protein expression (>2‑fold change) in NP69‑LMP1Δ232‑351 cells compared with NP69‑LMP1WT cells; and iii) LMP1WT was involved in activating the Janus kinase 3 (JAK3) promoter and regulating the expression of JAK3 protein, while LMP1Δ232‑351 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.