我们发现肺癌中δ-catenin 与转录抑制因Kaiso结合，增强了经典Wnt通路下游靶基因MMP7、MTA2和 CyclinD1 等转录，提示了δ-catenin /Kaiso很可能与Wnt 通路存在交叉对话。但在肺鳞癌发生发展过程中，δ-catenin/Kaiso 与经典Wnt信号通路如何协同促进肺癌侵袭的机制并不清楚。本项目拟通过检测肺鳞癌中δ-catenin、Kaiso与经典Wnt信号通路关键成员的表达，以及鳞癌间质中浸润炎症细胞，使用免疫组化、激光共聚焦、IP等方法，揭示δ-catenin 与 Kaiso 协同经典Wnt 通路的关键成员募集鳞癌间质中的炎性细胞并促进肺癌细胞侵袭转移、增殖等生物学行为的相关性。

We found that δ-catenin could enhance the transcription level of MMP7, MTA2 and CyclinD1 by the transcription factor Kaiso.Whereas,these genes are also the tagert ones of canonical Wnt pathway, suggesting that δ-catenin, might could up-regulate the activity of canonical Wnt pathway. However, how δ-catenin/Kaiso combinated with classical Wnt signal pathway accelerate invasion of lung squamous cancer is still unkonwn. This project intends to detect the expression of δ-catenin/Kaiso, and the key member of classical Wnt signal pathway,as well as the inflammatory cell in the stroma of lung SCC, by using immunohistochemistry, confocal laser microscope, immunoprecipitation to reveal the correlation beteween δ-catenin/Kaiso and canonical Wnt signaling pathway in recruit inflammatory cell in lung SCC, and thus . This project will enrich the relationship between the δ-catenin, Kaiso ,the canonical Wnt pathway and inflammatory stroma in lung SCC, and provide a new treatment taget for the prevention and treatment of lung SCC.