EBV与鼻咽癌恶性进程关系密切。干扰素诱导跨膜蛋白IFITM1能抑制多种病毒的感染和复制。我们前期发现IFITM1表达与鼻咽癌患者生存率呈正相关，并能抑制EBV的EBNA1、LMP1的表达和鼻咽癌细胞增殖，且IFITM1有可能与EGFR和EBV受体蛋白EphA2存在互作关系。据此，我们推测IFITM1有可能通过与EGFR、EphA2蛋白相互作用，抑制EBV感染和复制，进而影响鼻咽癌的恶性进展。因此，本项目拟：1) 从临床标本和细胞水平探索IFITM1抑制EBV感染与复制的作用及对鼻咽癌恶性进展的影响；2) 阐明IFITM1/EGFR/EphA2蛋白相互作用及抑制EBV的分子机制；3) 最后，在临床样本中验证IFITM1、EGFR、EphA2表达相关性和共定位关系，及其与EBV EBNA1、LMP1表达的相关性。本项目有望提出IFITM1抑制EBV感染与复制进而调控鼻咽癌恶性进程的新机制。

EBV is closely related to the malignant progression of nasopharyngeal carcinoma. Interferon-induced transmembrane protein IFITM1 can inhibit the infection and replication of a variety of viruses. We previously found that expression level of IFITM1 was positively correlated with survival rate of patients with nasopharyngeal carcinoma. And IFITM1 can inhibite the expression of EBV’s markers protein EBNA1, LMP1 and nasopharyngeal carcinoma cell proliferation. Interestingly, we also found IFITM1 can interact with EGFR and EBV receptor protein EphA2. Therefore, we speculated that IFITM1 may inhibit EBV infection and replication by interacting with EGFR and EphA2, thereby with affecting the malignant progression of nasopharyngeal cancer. Here, our project aims to: 1) explore the role of IFITM1 in inhibiting EBV infection and replication and its influence on malignant progression of nasopharyngeal cancer in clinical specimens and the cells; 2) clarify the protein-on-protein interaction of IFITM1/EGFR/EphA2 and their molecular mechanism of EBV inhibition; 3) finally, we will verify correlation and co-localization of IFITM1, EGFR and EphA2 and their correlation with EBV’s markers protein EBNA1 and LMP1 by clinical specimens. This project is expected to propose a new mechanism of IFITM1 on inhibiting EBV infection and replication to regulate the malignant process of nasopharyngeal carcinoma.