Regulation mechanism and function of Latent Membrane protein of Epstein-Barr Virus in nasal NK/T cell lymphoma cells.

鼻NK/T细胞淋巴瘤是EBV相关性恶性肿瘤，预后较差。我们已经证明，在鼻腔NK/T细胞淋巴瘤细胞系中，IL-2、10和15等细胞因子可以增强LMP-1的表达，LMP-1是EBV起源的癌蛋白。在本研究中，我们发现趋化因子IP-10(干扰素-γ诱导蛋白-10)是由LMP-1诱导的，并且IP-10以自分泌的方式增强细胞的侵袭能力。此外，我们还发现IP-10通过膜结合的IL-15通过细胞接触的方式促进单核细胞的增殖和LMP-1的表达。因此，LMP-1通过IP-10或单核细胞增强细胞的增殖和侵袭能力。

Nasal NK/T-cell lymphoma is EBV-related malignancy, and has a poor prognosis. We have already shown that an expression of LMP-1, EBV-originated oncoprotein, was enhanced by cytokines such as IL-2, 10, and 15 in nasal NK/T-cell lymphoma cell lines. In this study, we found that chemokine IP-10 (Interferon gamma-induced protein-10) was induced by LMP-1, and IP-10 enhanced invasive potential of the cells in autocrine manner. Moreover, we revealed that monocytes attracted by IP-10 enhanced proliferation and LMP-1 expression of the cells by cell-contact manner via membrane-bound IL-15. Therefore, LMP-1 enhanced the proliferating and invasive potential of the cells through IP-10 or monocytes.