IBDs 是多种病因引起的、异常免疫介导的肠道慢性、复发性炎症，长期慢性炎症增加肿瘤发生的风险，然而IBDs 癌变的确切机制尚不明确。申请人前期发现巨噬细胞等单核细胞在炎症诱导肿瘤中发挥了重要作用(第一作者,Cancer Cell,2013)，课题组前期研究提示 Calponin2可以调控巨噬细胞活化参与炎症反应，且申请人近期研究证实Calponin2参与消化系肿瘤的恶性生物学行为(通讯作者,Oncotarget,2017)。本课题拟结合临床标本、动物模型及细胞学实验，利用Calponin2-/-和对照小鼠的结肠炎、结肠炎相关性结肠癌动物模型，研究 Calponin2对结肠上皮细胞、免疫细胞的调控，特别是通过调控巨噬细胞，影响结肠炎和结肠炎相关结肠癌的发生发展，明确Calponin2参与消化系肿瘤发生发展的机制，为临床防治提供干预手段。

IBD is identified as a complex, remitting and relapsing inflammatory disorders that affecting the intestinal tract, with genetic and environmental risk factors. A serious consequence of long-term chronic inflammation is an increased risk of tumorigenesis. However, the exact pathogenesis of colitis associated cancer(CAC) is not fully understood. Applicant have found that macrophages and other monocytes have played an important role in inflammation-induced tumorigenesis (first author, Cancer Cell, 2013). Previous studies had proved that Calponin 2 participated in inflammatory response by inhibiting macrophage activation, and applicant found that Calponin 2 involved in the pathogenesis of GI cancer (Corresponding Author, Oncotarget，2017).In this study, we aim to investigate the mechanism of how Calponin 2 affect colitis and CAC by regualting colonic epithelial cells and immune cell, especially macrophage, and propose the possible methods of clinical intervention.