慢性炎症微环境在诱发肿瘤发生过程中发挥关键性的作用，肠道异常活化的免疫细胞可导致肠道上皮细胞恶变，深入研究结肠炎-癌转化过程中细胞及细胞因子之间的相互作用不论对肠道免疫系统还是对结肠炎-癌转化的分子机理认识都具有非常重要的意义。本项目拟围绕结肠炎-癌转化过程中白细胞介素家族IL-6/IL-17介导的信号通路，研究结肠上皮细胞与TH17细胞的相互作用及其在炎症向肿瘤恶变过程中的功能；研究结肠炎-癌转化过程中IL-6诱导TH17细胞分化产生IL-17的分子机制；研究IL-17激活上皮细胞分泌IL-6的正反馈信号通路以及该信号通路在慢性肠炎向结肠癌转化中的功能。希望通过本项目研究，深入阐明结肠炎-癌转化的分子机制，为非可控性结肠炎恶性转化提供新的可能干预靶点和治疗思路。

The microenvironment formulated by chronic inflammation plays a key role during the process of tumorigenesis. Aberrantly activated colonic immune cells can lead to the malignant transformation of colonic epithelial cells. Intensively investigating the interaction between cells and cytokines during the process of colitis associated colorectal cancer has important significance in realizing the colonic immune system and the molecular mechanism of malignant transformation. In this project, we will focus on the regulation of interleukin family (IL-6/IL-17)-mediated signaling pathways during the chronic colitis-associated malignant transformation. The interaction between colonic epithelial cells and TH17 cells and its biological function in malignant transformation will be studied: investigating the basis of IL-6 in inducing TH17 cell differentiation and the secretion of IL-17; the positive feedback signaling pathway of IL-17 in promoting the secretion of IL-6 by epithelial cells and the role of this pathway in chronic colitis mediated malignant transformation. The study of the regulatory network will not only provides new theoretical evidences for the malignant transformation basis during colitis-associated malignant transformation, but also provide novel targets and therapeutic clues for the clinical treatment of uncontrolled colitis-associated malignant transformation.