CMTM1原命名CKLFSF1，是本课题组自主克隆得到的新基因，于2004年在国际上首次进行了报道。CMTM1结构复杂，共23个剪切变异体，CMTM1-v5是其中一个剪切体。前期研究结果表明CMTM1-v5能够特异性进入淋巴瘤细胞株Raji、Jurkat细胞，抑制细胞增殖和诱导细胞凋亡，抑制NF-κB信号通路。本课题将在前期研究工作的基础上，继续诱导、表达、纯化大量人重组CMTM1-v5蛋白，对该蛋白在细胞水平和动物体内功能与机制进行深入研究。主要研究内容包括：CMTM1-v5特异性进入淋巴瘤细胞株Raji、Jurkat的途径和机制，进入细胞后的定位以及相互作用分子；诱导细胞凋亡的作用机制；在NF-κB信号通路中的作用节点；确定人重组CMTM1-v5蛋白在动物体内的抗瘤作用以及生存期的变化。本项研究属于源头创新，可以为淋巴瘤的靶向新药研发提供实验依据，具有重要的理论意义和临床应用价值。

CMTM1, original named CKLFSF1, is a new gene cloned by using bioinformatics approach. We first reported which in the international arena in 2004 and we got the independent intellectual property rights as well. The structure of the gene is complex, consist of 23 isoforms, named as CMTM1-v1 to v23 separately, thereinto, CMTM1-v5 is one of these isoforms. Luciferase reporter gene assay shows that CMTM1-v5 is able to inhibit the activation of NF-κB. In the other hand, related CCK8 and apoptosis detection indicates that both overexpression and recombinant human CMTM1-v5 can not only inhibit proliferation but also induce apoptosis in Raji cell and Jurkat cell. This project will conduct in-depth study to CMTM1-v5 of mechanism in lymphoma cells line Raji, Jurkat. We will adopt yeast two-hybrid, co-immunoprecipitation and co-localization to look and confirm the interaction of molecules. We will research the node of CMTM1-v5 in NF-κB signaling pathway, and the induced apoptosis mechanism; we are going to clarify recombinant human CMTM1-v5 ways into the target cell. We are going to determine recombinant human CMTM1-v5 anti-tumor effect in local and systemic in vivo injection of Raji cells, as well as the survival of change lymphoma systemic damage. We are going to provide experimental evidence for clinical research of lymphoma and a new candidate molecules for the targeted therapy of the disease. Therefore, this series of research has vital theoretical significance and application value as the source of innovation.