胆管癌侵袭转移能力强、手术切除率低、预后差，是外科界的一道难题。我们在前期研究中筛选并鉴定出Stathmin蛋白质在胆管癌中高表达。而近期研究认为其和肿瘤进展密切相关。进一步的预实验结果提示Stathmin促进胆管癌细胞侵袭迁移且和上皮间质转化( epithelial-mesenchymal transition,EMT)相关，但其作用机制仍不明确。为此我们提出假说：Stathmin通过调控整合蛋白/FAK信号通路促使胆管癌发生EMT，从而促进侵袭转移。本项目拟通过人胆管癌EMT细胞模型、裸鼠移植瘤模型和人胆管癌组织芯片，采用RNA干扰、Western blot等技术，从体外到体内、从基础到临床多方位验证假说，旨在阐明Stathmin调控整合蛋白/FAK信号通路在胆管癌EMT中的作用，探索其分子机制，以期为胆管癌的临床诊治提供新的预测指标和治疗靶点。

Cholangiocarcinoma has a strong ability of invasion and metastasis, low rate of excision and poor prognosis. It is a difficult problem for the realm of surgery. Stathmin is highly expressed in cholangiocarcinoma and it had been selected and identified in our preliminary research. It has been considered to have a great relationship with the progress of tumor in recent researches. Further research indicate that Stathmin promote invasion and metastasis of cholangiocarcinoma cell and related to epithelial-mesenchymal transition(EMT), however the mechanism is still unknown. Therefore we suppose that Stathmin promote EMT of cholangiocarcinoma via regulating integrin/FAK singal pathway and then it promote invasion and metastasis. We hope to clarify the effect of stathmin regulating integrin/FAK singal pathway in EMT of cholangiocarcinoma, quest for the molecular mechanism via EMT model of cholangiocarcinoma cell，transplantation tumor model in nude mice and human cholangiocarcinoma tissue microarray in this program, using RNAi and western blot technique, from vivo to vitro, from basic to clinic, expecting to find a new prognosis index and therapeutic target for diagnosis and clinical treatment of cholangiocarcinoma.