由于胃癌的高转移、高复发性等特点，迫切需要寻找新的治疗靶点。前期研究发现Trop2在胃癌中高表达，与胃癌病人预后及vimentin的表达相关；细胞学实验发现Trop2能促进胃癌细胞的增殖、迁移、侵袭，并能诱导胃癌EMT现象；生物信息学分析和pull down实验提示Trop2和β-catenin存在物理结合，并可能激活Wnt信号通路。因此我们提出“Trop2激活β-catenin通过Wnt信号通路促进胃癌EMT和侵袭转移”这一科学假说。本项目拟结合体内外实验，证明Trop2在胃癌侵袭转移中的作用，应用Co-IP, CHIP等技术结合拯救实验，阐明Trop2激活β-catenin通过Wnt信号通路促进胃癌EMT和侵袭转移的分子机制。经文献检索，国内外尚未见相关报道，本研究有望明确Trop2作为胃癌新的治疗靶点，加深对胃癌侵袭转移分子机制的阐明，为胃癌的精准治疗提供理论基础和实验依据。

The gastric cancer (GC) has the characteristics of high metastasis and high recurrence. Moreover, the targeted therapy for GC has not achieved obvious effect, it is urgent to find novel target for GC. Our previous study indicated that Trop2 was over-expressed in GC and associated with poor overall survival rates of GC patients, moreover, the relationship between the expression level of Trop2 and that of vimentin was positively correlated . We also found that Trop2 could induce proliferation, migration, invasion and EMT of GC in vitro. Bioinfomatic analysis and pull-down experiment indicated that Trop2 could bind with β-catenin and play a role in activating Wnt signaling pathway. Based on above results, we therefore hypothesize that Trop2 promotes epithelial–mesenchymal transition and metastasis of gastric cancer by activating Wnt /β-catenin signaling pathway. In this study, we would clarify the role of Trop2 in invasion and metastasis of GC both in vivo and in vitro. We plan to analysis the molecular mechanism of Trop2 to induce EMT and promote the invasion and metastasis of GC by activating Wnt/β-catenin signaling pathway. Up to now, there is no report about Trop2’s regulating Wnt/β-catenin signaling pathway of GC. Our study could provide Trop2 as a new potential biomarker for GC, bring a better understanding of the molecular mechanism of invasion and metastasis of GC, and may also provide the theoretical and experimental basis for precision treatment of GC.