c-Jun N-末端激酶信号转导通路调节细胞迁移的机制

摘要

c-Jun N-末端激酶（JNK）是促丝裂原激活蛋白激酶家族成员，转导细胞外信号为细胞内反应。JNK信号通路主要被细胞因子和应激刺激激活，调节细胞迁移，参与细胞增殖、分化、炎症和程序性死亡。细胞迁移机制与细胞骨架、黏着斑、黏着斑激酶、整联蛋白、鼠肉瘤病毒同源癌基因家族蛋白、G-蛋白和水通道蛋白等紧密相关，但其调控机制尚不清楚。目前JNK通路调节细胞迁移的研究显示：在上皮和成纤维细胞，JNK信号通路被活化，可促进细胞迁移，增强伤口愈合、组织修复；在肿瘤细胞，JNK信号通路被抑制可降低肿瘤细胞的迁移能力；在炎症环境下，JNK的作用与机制表现出差异性，有待进一步研究。诠释JNK信号转导通路参与调节细胞迁移的具体机制可为组织修复、炎症控制和肿瘤治疗提供新的思路。%C-Jun N-terminal kinase(JNK) is a member of the mitogen-activated protein kinase family, which regulates diverse cellular programs by relaying extracellular signals to intracellular responses. Activated primarily by cytokines and environmental stress, the JNK signal transduction pathway regulates cell migration and plays an important role in cellular proliferation, differentiation, inflammatory response, and apoptosis. The mechanism of cell migration is closely related to the cytoskeleton, focal adhesion, focal adhesion kinase, integrin, and ras homology oncogene family proteins, G-protein, and aquaporin. Recent research on JNK pathway regulating cell migration shows that the activation of the JNK signaling pathway can promote epithelial cell and fibroblast migration and can enhance wound healing and tissue repair. Inhibiting the JNK signaling pathway can reduce cell migration and invasion in tumor cells. The function and mechanism of JNK in inflammation are controversial. Discovering the specific mechanisms underlying the activities of the JNK signal transduction pathway, which is involved in regulating cell migration, can provide new ideas for tissue repair, inflammation control, and tumor treatment.