胰腺癌恶性程度高，预后极差。胰腺癌肿瘤微环境中产生的细胞因子在肿瘤的进展中扮演重要角色，但其作用靶点及发生机制尚不清楚。白介素22（Interleukin22，IL-22)不仅参与炎症和修复过程，而且参与恶性肿瘤的进展过程。我们前期研究发现高表达IL22及其受体与胰腺癌淋巴结侵犯及预后不良相关，STAT3信号通路参与了这一过程。IL-22不仅在胰腺癌组织中明显高表达，而且主要表达于胰腺癌组织的间质中。进一步发现IL-22干预能促进胰腺癌细胞上皮-间质转变（EMT）的发生。以上结果提示IL-22很可能通过胰腺癌微环境中间质细胞促进胰腺癌恶性进展及EMT的形成。我们拟通过临床病理学分析，利用基因转染及基因沉默技术，进行体外共培养和体内成瘤实验，对胰腺星状细胞高表达IL-22促进胰腺癌细胞侵袭转移及EMT形成进行深入研究，可望阐明相应的分子机制，为胰腺癌的综合治疗提供新的策略和靶点。

Pancreatic cancer is one of the most aggressive cancers. The cytokines produced by the microenvironment of pancreatic cancer play a critical role in progression of tumor, but the target and mechanism is unclear. IL-22 is a cytokine involved not only in inflammatory and healing processes, but also in malignant disease progress. Our previous study found that high expression of IL-22 and IL-22R was associated with lymphatic metastasis and poor prognosis. IL-22 is not only expressed in tissue of pancreatic cancer, but also mainly in mesenchyma of pancreatic cancer. Furthermore, we found that IL-22 promote EMT formation of pancreatic cancer cells. These results suggest that IL-22 can promote the progression of pancreatic cancer and EMT formation. We will study the mechanism which pancreatic stellate cell promote invasion and metastasis of pancreatic cancer by clinical and pathological analysis, gene transfection and gene silencing technology. It might clarify molecular mechanism and provide new therapeutic strategy and target for pancreatic cancer.