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.

In the present study, the interaction of proteins in the microenvironment of gastric mucosal atypical hyperplasia was analyzed. The stromata of normal gastric mucosa (NGM) and gastric mucosal atypical hyperplasia (GMAH) tissues were purified with laser capture microdissection (LCM). The differentially expressed GMAH proteins of the NGM and GMAH tissues were identified by quantitative proteomic techniques with isotope labeling. The cross-talk between differentially expressed proteins in NGM and GMAH tissues was then analyzed by bioinformatics. There were 165 differentially expressed proteins identified from the stromata of NGM and GMAH tissues. Among them, 99 proteins were upregulated and 66 were downregulated in GMAH tissue. The present study demonstrated that these proteins in gastric mucosal atypical hyperplasia were involved in cancer-associated signaling pathways, including the p53, mitogen-activated protein kinase (MAPK), cell cycle and apoptosis signaling pathways, and were involved in cellular growth, cellular proliferation, apoptosis and the humoral immune response. The results of the present study suggest that the 165 differentially expressed proteins, including S100 calcium-binding protein A6 (S100A6) and superoxide dismutase 3 (SOD3) in the microenvironment of gastric mucosal atypical hyperplasia, are involved in the p53, MAPK, cell cycle and apoptosis signaling pathways, and serve a function in the pathogenesis of gastric cancer.