目前肿瘤免疫逃逸作为恶性肿瘤的重要标志之一，且鼻咽癌的发生发展与肿瘤细胞的免疫逃逸密切相关，重建抗肿瘤免疫监控是近年来研究的热点。本课题组前期研究证实PBK促进鼻咽癌发生发展，进一步通过高通量筛选鉴定PBK上调B7家族免疫相关分子CD276（B7-H3），因此我们提出PBK上调CD276促进鼻咽癌免疫逃逸的科学假说，通过应用生物信息学分析、IP-银染-质谱、CHIP-QPCR实验、动物模型和FACS分析浸润淋巴细胞比例等，本项目将进一步证实 MSL1参与PBK调控CD276，揭示PBK/MSL1轴上调CD276 mRNA转录的分子机制，阐明CD276介导鼻咽癌免疫逃逸的作用，探索CD276作为肿瘤免疫治疗新靶抗原的潜力，为鼻咽癌精准治疗和进一步提高治愈率奠定理论基础。

As the hallmark of malignant tumor, tumor immune evasion is closely related to the development and progression in nasopharyngeal carcinoma, immune surveillance reconstitution is the focus recently. Our previous study revealed that the PBK promoted progression in NPC, further high-throughput screening exploration found that PBK upregulated CD276（B7-H3）, we propose the hypothesis that PBK promotes NPC evading immune destruction by increasing CD276. In the present proposal, we will use bioinformatics analysis, IP-silver staining-mass spectroscopy, CHIP-QPCR、tumor animal model and infiltrating lymphocytes percentage in FACS analysis research aims, we will determine that MSL1 participate in regulation of CD276 by PBK, reveal the molecular mechanism of increasing in CD276 mRNA transcription which regulated by PBK/MSL1 axis, illuminate the role of CD276 in NPC immune evasion, these findings will explore the potential of CD276 as the new target antigen in immunotherapy of NPC, and aid in the development of accurate treatment and survival benefit for the NPC patients.