肿瘤转移是胰导管细胞癌（PDAC）致死的主要原因，但发生机制仍不明确。趋化因子Fractalkin（FKN）具有黏附与趋化的双重生物学功能，可通过与其受体CX3CR1相互作用介导肿瘤转移的发生。我们的预实验发现，PDAC患者血清中FKN的表达与PDAC的病理分期程度呈正相关。由于Jak/STAT信号途径中STAT3的异常激活与肿瘤形成密切相关，且我们以往的研究指出FKN是调控Jak/STAT信号通路的重要分子，结合该项目的预实验结果，推测FKN可做为检测胰腺癌发生甚至转移的检测指标，其通过调控Jak/STAT信号通路中STAT3的活化，进而促进PDAC的转移。本课题拟以FKN及其受体CX3CR1做为研究对象，探讨FKN/CX3CR1轴与PDAC发生发展的重要相关性及其通过调控Jak/STAT信号传导途径促进肿瘤转移的明确作用机制，以期为临床上胰腺癌转移的作用机制提供新的理论依据和干预策略。

Metastasis is the major cause of death in pancreatic duct cell carcinoma (PDAC), but the pathological mechanism remains unclear. With dual biological function of both adhesion and chemotaxis, the chemokine Fractalkin (FKN) may mediate tumor metastasis through the interaction with CX3CR1. In our preliminary study, we found that the expression of FKN, membrane FKN and soluble FKN in serum of pancreatic cancer patients have a positive correlation with the pathological staging in PDAC. The abnormal activation of STAT3 in Jak/STAT signaling pathway is closely related with tumor development, and we have previously demonstrated that FKN is an essential factor in the regulation of Jak/STAT signaling pathway. Therefore, we presume that FKN could be used as a diagnostic marker in pancreatic cancer, and FKN may promote the tumor metastasis by activating STAT3 in PDAC. In the present study, we will focus the two specific forms of FKN and its receptor CX3CR1, and further investigate the correlation between FKN/CX3CR1 system and PDAC, as well as the mechanisms of regulation by Jak/STAT signaling pathway in tumor metastasis. We hope this project will provide a novel theoretical basis for the treatment of tumor metastasis in pancreatic cancer.