TRIM67在肿瘤中的表达及作用机制尚无报道。前期研究发现，TRIM67在非小细胞肺癌中高表达，且与高pTNM分期，淋巴结转移、肿瘤大小、分化程度及不良预后密切相关；TRIM67通过促进Notch信号通路影响肺癌细胞的增殖、迁移和侵袭。通过免疫共沉淀发现TRIM67与DLK1可以相互作用，从而影响非经典Notch通路活性，DLK1是Notch通路受体Notch1的抑制剂，因此我们推测TRIM67可能通过泛素化降解DLK1，抑制DLK1的表达，从而促进Notch通路活性，促进肺癌细胞恶性表型。本项目拟研究TRIM67通过与DLK1相互作用，激活Notch通路活性的机制；并研究TRIM67在体内的作用情况。本项目能明确TRIM67促进非小细胞肺癌增殖，迁移和侵袭的新机制，为肺癌的治疗提供新途径，为寻找新的非小细胞肺癌生物标记物和开发靶向药物提供实验基础。

The expression and mechanism of TRIM67 in tumors have not been reported. Previous studies have found that TRIM67 is highly expressed in non-small cell lung cancer and is closely related to advanced pTNM stage, lymph node metastasis, tumor size, degree of differentiation, and poor prognosis; TRIM67 affects the proliferation, migration, and invasion of lung cancer cells by promoting the Notch signaling pathway. Co-immunoprecipitation revealed that TRIM67 and DLK1 can interact to affect Notch pathway activity. DLK1 is an inhibitor of Notch pathway receptor Notch1. Therefore, we speculate that TRIM67 may degrade DLK1 through ubiquitination and inhibit DLK1 expression, thereby promoting Notch pathway and promoting the malignant phenotype of lung cancer cells. This project intends to study the mechanism by which TRIM67 activates the activity of Notch pathway through interaction with DLK1; and study the effect of TRIM67 in vivo . This project can clarify the new mechanism of TRIM67 promoting proliferation, migration and invasion of non-small cell lung cancer, and provide a new way for the treatment of lung cancer, providing us a potential target of clinical intervention for patients suffering lung cancer.