我们通过对特异性去SUMO化蛋白酶1（SENP1）敲除小鼠分析，发现SENP1能调控IFN-g对巨噬细胞的激活。用SENP1-/-骨髓移植小鼠肿瘤模型发现SENP1能调节肿瘤炎症反应与肿瘤转移。同时，我们还发现SENP1在结肠癌间质中包括一些炎症细胞中高表达。因此，我们提出SENP1通过调控炎症反应在结肠癌发生发展过程中有十分重要的作用。在本课题中，我们将对如下科学问题进行研究： 1. SENP1调控炎症反应对结肠癌发生发展的作用；2. SENP1调控肿瘤炎症反应的分子基础；3.协调SENP1的表达和调控炎症反应的分子机制；4. SENP1调控肿瘤炎症反应的临床意义。 对这些问题的回答，将使我们在了解SENP1调控肿瘤炎症反应的分子机制的基础上，进一步认识与理解SENP1在肿瘤发生发展中的作用和意义，以及SENP1作为治疗靶标在肿瘤临床中应用的可能性与策略。

In our previous studies, we found that SENP1 was essential for macrophages activated by IFN-?. By using SENP1-/- bone marrow transplant-tumor mouse model, we found that SENP1 could regulate tumor inflammatory reaction and tumor metastasis. We also detected the over-expression of SENP1 in the stroma of colon cancer samples. Therefore, we propose that SENP1 may play a crucial role in colon cancer through the regulation of tumor inflammation. We will perform experiments to determine: 1). the role of SENP1 in tumor inflammation during colon cancer development; 2). The mechanism underlying SENP1 regulation of inflammation; 3). How to regulate SENP1 expression during inflammation? 4). What is the clinical significance of SENP1 regulation of inflammation? These studies will provide insight into tumor inflammation.