胃癌的浸润和转移是导致患者死亡的主要原因。胃癌的转移是多基因、多步骤、多信号传导通路异常的共同结果。深入探索胃癌浸润、转移的机制，对胃癌的早期诊疗寻找有效的分子靶点尤为重要。我们的研究表明，KIF26B作为癌基因与胃癌患者的预后直接相关；且KIF26B在细胞增殖、迁移、浸润中发挥重要作用。基于此本课题继续研究KIF26B 3’UTR对KIF26B异常表达的影响；明确KIF26B 3’UTR在体外细胞学及体内动物中发挥的生物学功能；研究KIF26B 3’UTR与RNA结合蛋白协同调控KIF26B表达的分子机制。初步结果显示，外源性KIF26B 3’UTR调控KIF26B的表达，且能够结合STAU1、CUL4B等RNA结合蛋白发挥促进细胞浸润、转移的作用。本课题将为胃癌的转移机制及早期诊疗提供重要理论依据及新的策略。

Invasion and metastasis of gastric cancer is the leading cause of death in patients. The process of gastric cancer invasion and metastasis is a result of abnormal genes and signaling pathways, which formed a complex network to affect the occurrence of tumor metastasis on different levels. To explore the mechanism of metastasis and to find new therapeutic targets have become current research focus in gastric cancer. In our previous studies, we found that increased expression of KIF26B was correlated with larger tumor size, positive lymph node metastasis, or distant metastasis and poorer prognosis. KIF26B could facilitate invasion and metastasis of gastric cancer cells in vitro and in vivo. Based on the above results, we will investigate the roles of KIF26B 3’-untranslated regions UTR (3’UTR) in regulating oncogene KIF26B expression. In addition, we study the biological function of KIF26B 3’UTR. Furthermore, we will gain insights into the molecular mechanisms by which KIF26B 3’UTR coordinates with RNA binding protein to regulate gastric cancer metastasis. In our preliminary results, we found that KIF26B 3’UTR upregulated KIF26B mRNA and protein expressed levels. And KIF26B 3’UTR bind STAU1or CUL4B RNA binding protein to promote gastric cancer cells invasion and migration. Therefore, this study will provide important new strategies on the diagnosis and treatment of gastric cancer metastasis.