鼻咽癌（NPC）转移是制约患者预后的重要因素，肿瘤血管生成与NPC转移密切相关。课题组前期研究及相关报道显示NPC来源的外泌体可促进血管生成。本课题预实验发现富含miR-23a的外泌体与NPC转移相关；且可改变肿瘤微环境中血管内皮细胞（HUVECs）的生物学行为、促进肿瘤血管生成。据此提出：富含miR-23a的外泌体通过调控肿瘤血管生成来促进NPC转移。本课题拟首先利用PCR技术验证NPC患者血液来源的外泌体中miR-23a表达水平与转移的关系；然后在细胞水平分析富含miR-23a的外泌体对血管生成的影响；接着研究miR-23a对血管生成的作用，并用荧光素酶报告基因实验验证其下游靶分子, 阐明表型产生的分子机制；最后利用斑马鱼模型验证上述假说。本研究有助于阐明NPC转移的分子机制，为判断NPC患者预后并进行个体化治疗提供新的科学依据。

Metastasis is the major cause of poor prognosis among NPC patients. And tumor angiogenesis is closely associated with the metastasis of NPC. Previous studies and our research had both showed that exosomes could promote tumor angiogenesis. Surprisingly, we found that increased serum levels of circulating exosomal miR-23a was related to metastasis in NPC patients, and overexpression of exosomal miR-23a could change the biological behavior of HUVECs and promote NPC angiogenesis. In view of this, we speculated that high expression of exosomal miR-23a could promote NPC angiogenesis and accelerate the metastasis of NPC. In the present study, we will first use PCR to explore the expression of the serum levels of exosomal miR-23a in NPC patients and find its association with metastasis. Then we will investigate the impact of miR-23a containing exosomes on tumor angiogenesis in cell lines. After that, we will determine the roles of miR-23a in tumor angiogenesis and look for the mechanism. Finally, we will verify our speculation with zebrafish. Our investigation might help clarify the molecular mechanism of NPC metastasis and provide potential opportunity for NPC therapy.