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中文摘要：
摘要人类鼻咽黏膜表面的分泌物中富含天然免疫蛋白，腭、肺及鼻咽上皮克隆（palate，lung and nasal epithelium clone，PLUNC）蛋白家族成员SPLUNCl和LPLUNCl就是其中的重要组成部分，这两个蛋白在鼻咽上皮相对特异高表达，它们都具有杀菌／渗透增强蛋白（bactericidal／permeability-increasing protein，BPI）结构域，可通过BPI结构域与细菌脂多糖（1ipopolysaccharides，LPS）结合从而直接杀灭或抑制细菌生长，也可以有效抑制EB病毒（Epstein．Barrvirus，EBV）等致癌微生物对鼻咽上皮的侵袭从而发挥其免疫防御功能．它们还可以通过抑制IL-6等炎症因子的分泌和NF．KB、STAT3等炎症相关通路的激活，阻止鼻咽部的慢性炎症反应及鼻咽上皮的恶性转化．在鼻咽癌细胞中重新表达PLUNC蛋白，可以通过促分裂素原活化蛋白激酶（Mitogen．activatedproteinkinase，MAPK）或miR．141．PTEN—AKT等信号通路抑制鼻咽癌细胞的增殖，促进鼻咽癌细胞的凋亡．进一步深入研究PLUNC蛋白家族在鼻咽癌发病中的作用机制，对指导鼻咽癌的防治具有蕈要的意义．
英文摘要：
Secretion on the surface of human nasal mucosa contains many innate proteins, the key factors of which are SPLUNC1 and LPLUNC1, members of the palate, lung and nasal epithelium clone （PLUNC） family. These two proteins are highly expressed in nasopharyngeal epithelium with the relative specificity. Both of them have bacterial/permeability-increasing protein （BPI） domain which can bind to lipopolysaccharide （LPS） to inhibit or kill bacterial growth directly. They also have the immuno defense function to protect nasopharyngeal epithelium from Epstein-Barr virus （EBV） and some other pathogenic microorganism effectively. These proteins play a significant role in the process of chronic inflammation and carcinogenesis of nasopharyngeal epithelium by inhibiting the secretion of inflammatory factors, such as IL-6, through activating NF-KB and STAT3 signaling pathways. In addition, they also can suppress nasopharyngeal carcinoma （NPC） cell growth and induce cell apoptosis through MAPK and miR-141-PTEN-AKT signaling pathways when the PLUNC proteins are re-expressed in NPC cell lines. Further study about the mechanism of PLUNC protein family in pathogenesis of NPC has important significance for the prevention and treatment guidance of NPC.
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