Epstein–Barr virus (EBV) is positively related to the morbidity of nasopharyngeal carcinoma (NPC) in Asia. After infection, EBV can produce several proteins, including viral interleukin‐10 (vIL‐10). But the mechanism by which vIL‐10 contributes to NPC cell proliferation and cell cycle progression is not well understood. In this study, EBV negative and positive cell lines, and the JAK2/STAT3 signal pathway inhibitor AG490 were used to illustrate the role of vIL‐10 in NPC. Cell proliferation and cell cycle were measured by CCK‐8 and flow cytometry. The expression levels of related protein were measured by Western blotting. High concentrations of vIL‐10 and IL‐6 were found in the EBV positive patients. The expression level of IL‐6 was positively related to the presence of concentration of vIL‐10. vIL‐10 can promote cancer cell proliferation and G1 to S phase transmission via upregulating the IL‐6 protein level by activating the JAK2/STAT3 signal pathway. Furthermore, EBV can induce the formation of cytotoxic T cells, whereas vIL‐10 can block the function of cytotoxic T cells. Taken together, these results suggest that vIL‐10 promotes cell proliferation and cell cycle progression via JAK2/STAT3 signaling pathway in NPC.

中文翻译：

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病毒IL-10通过JAK2 / STAT3信号通路促进鼻咽癌细胞中的细胞增殖和细胞周期进程。

爱泼斯坦巴尔病毒（EBV）与亚洲鼻咽癌（NPC）的发病率呈正相关。感染后，EBV可产生多种蛋白质，包括病毒白介素-10（vIL-10）。但是，vIL-10促进NPC细胞增殖和细胞周期进程的机制尚不十分清楚。在这项研究中，EBV阴性和阳性细胞系以及JAK2 / STAT3信号途径抑制剂AG490被用来说明vIL-10在NPC中的作用。通过CCK-8和流式细胞仪测量细胞增殖和细胞周期。通过蛋白质印迹法测量相关蛋白的表达水平。在EBV阳性患者中发现高浓度的vIL-10和IL-6。IL-6的表达水平与vIL-10的浓度呈正相关。vIL-10可通过激活JAK2 / STAT3信号通路来上调IL-6蛋白水平，从而促进癌细胞增殖和G1至S期的传播。此外，EBV可以诱导细胞毒性T细胞的形成，而vIL-10可以阻断细胞毒性T细胞的功能。综上所述，这些结果表明，vIL-10通过NPC中的JAK2 / STAT3信号通路促进细胞增殖和细胞周期进程。