胰腺癌干细胞(pancreatic cancer stem cells, PCSC)是高度恶性肿瘤之一的胰腺癌治疗失败的关键“元凶”。肿瘤微环境中的M2巨噬细胞是促进胰腺癌恶化和维持PCSC干性的重要因素。我们前期研究发现，胰腺癌中高表达的趋化因子Fractalkine（FKN）具有趋化M2巨噬细胞的作用，但二者是否引起胰腺癌恶化和维持PCSC干性，目前尚不清楚。因此，本研究首先确认FKN、M2巨噬细胞浸润水平同胰腺癌临床参数的相关程度，然后通过过表达或敲减FKN，并合并M2巨噬细胞共培养，来观察二者对胰腺癌干细胞特性、上皮间质转化(epithelial-mesenchymal transition, EMT)，以及在胰腺癌荷瘤小鼠模型上的体内影响。本项目旨在加深对胰腺癌恶性复发机制的了解，并寻找阻断胰腺癌干细胞特性的胰腺癌治疗靶点。

Pancreatic cancer stem cells (PCSC) are the "prime culprit" of failure treating pancreatic carcinoma (PC), which remains one of the most challenging malignant tumors. According to the reported literatures, infiltration of M2 macrophages into tumor microenvironment exerts key role in promoting metastasis and maintaining characteristics of cancer stem cells (CSC). In our previous study, we found that FKN overexpression could recruit M2 macrophages. Accordingly, it still needs deeply exploration for the role of combination of FKN overexpression and M2 infiltration in metastasis and CSC characteristics. In this project, we will confirm the correlation of FKN expression or M2 infiltration with PC clinical parameters firstly. Then, it is observed the in vitro and in vivo effects on preservation of PCSC properties, epithelial-mesenchymal transition (EMT) using co-culture of M2 with PC cells overexpressing or siliencing FKN. The meaningfulness of this study is to find new PC targets, and to explore its action for PCSC pathogenesis.