SUMO特异性蛋白酶1(SENP1)与淋巴瘤发生的关系不清楚。我们前期发现SENP1在人套细胞淋巴瘤（MCL）中高表达，干扰SENP1显著抑制MCL细胞增殖和克隆形成能力。利用Micro-array发现干扰SENP1导致MCL发病相关重要基因BTK表达下调，并且SENP1可促进BTK启动子活性。生物信息学预测BTK启动子区有转录因子ZNF521的结合位点，而SENP1能去除ZNF521的SUMO1修饰、促进其入核。据此提出假设：SENP1通过去除ZNF521的SUMO1修饰促进ZNF521入核，上调BTK表达促进MCL发生。本研究将解析SENP1促进ZNF521入核上调BTK的分子机制；体外探讨SENP1-ZNF521-BTK轴对MCL细胞生物学特征的影响；荷瘤裸鼠模型探讨该轴对MCL成瘤的影响，以期揭示SENP1-ZNF521-BTK轴是参与MCL发生的新机制，为MCL防治提供新靶标。

The association between SUMO-specific proteases 1 (SENP1) and the development of lymphoma is unclear. We found that SENP1 was highly expressed in human mantle cell lymphoma (MCL) tissues and MCL cell lines, and silencing of SENP1 expression in MCL cells dramatically inhibited the cell proliferation and colony formation. Based on the comparison of gene expression profile Using Micro-array, we found that silencing of SENP1 expression in MCL silencing of suppressed the expression of BTK, which is a key gene involved in the development of MCL. Moreover, SENP1 increased the activity of the promoter of BTK. Bioinformatics suggests that there is a binding site of transcription factor zinc finger protein 521 (ZNF521) during BTK promoter, and SENP1 regulated SUMOylation of and supported ZNF521 nuclear retention. Taken together, we hypothesize that SENP1 may induce BTK expression and eventually promote MCL development via regulating SUMOylation of ZNF521. In the present study, we will explore the mechanism by which SENP1 regulates BTK expression via ZNF521. Then, we will analyse the effects of SENP1-ZNF521-BTK axis on the biological characteristics of MCL cells from in vitro experiments. Furthermore, we will construct tumor-bearing mice to investigate the in vivo effects of this axis on MCL development. Through the above research, it is expected to reveal that the axis may be a novel mechanism to participate in the development of MCL, which may provide a novel target for the prevention and treatment of MCL.