胃癌的转移和侵袭特性是威胁患者生存的重要因素。我们的前期工作发现TPX2可以促进胃癌的转移和侵袭，但其机制不清楚。进一步的表达谱筛选与分析发现：（1）ITGA6作为TPX2的下游参与胃癌转移和侵袭的调控；（2）TPX2对JNK/AP-1通路有调控作用；（3）AP-1作为转录因子可以和ITGA6的启动子结合从而调控ITGA6的表达。因此，TPX2可能通过JNK/AP-1通路调控ITGA6的表达从而影响胃癌的转移和侵袭能力。本项目拟利用细胞与分子生物学技术，通过动物与细胞模型，结合临床标本，同时设计系列Rescue实验，进一步明确：（1）ITGA6在胃癌转移和侵袭中的作用；（2）AP-1对ITGA6表达的调控；（3）TPX2是否通过JNK/AP-1调控ITGA6表达，从而影响胃癌的转移和侵袭。以期为胃癌转移和侵袭的病理机制提供新观点，为抑制胃癌转移提供新的潜在药物靶点。

The metastasis and invasion of gastric cancer is an important factor threatening the survival of patients. Our previous work has shown that TPX2 can promote the metastasis and invasion of gastric cancer, but its mechanism is unclear. Further expression profiles were screened and analyzed: (1) ITGA6 as a downstream of TPX2 is involved in the regulation of gastric cancer metastasis and invasion; (2) TPX2 has a regulatory role for the JNK/AP-1 pathway; (3) AP-1 as a transcription factor can bind to the promoter of ITGA6 to regulate the expression of ITGA6. Therefore, TPX2 may regulate the expression of ITGA6 through JNK/AP-1 pathway and thus affect the ability of metastasis and invasion of gastric cancer. This project intends to use cell and molecular biology technology, through animal and cell models, combined with clinical specimens, while designing a series of Rescue experiments to further clarify: (1) The role of ITGA6 in metastasis and invasion of gastric cancer; (2) Regulation of ITGA6 expression by AP-1; (3) Whether TPX2 through JNK/AP-1 regulation of ITGA6 expression, thus affecting the metastasis and invasion of gastric cancer. The aim of this study is to provide a new perspective for the pathological mechanism of metastasis and invasion of gastric cancer, and to provide a new potential drug target for inhibiting the metastasis of gastric cancer.