TANK 结合激酶 1 (TBK1) 是 IKK 家族的成员，在非经典 NF-κB 信号传导和 I 型干扰素反应的激活中发挥着至关重要的作用。 TBK1 的异常激活有助于各种类型肿瘤细胞的增殖和存活，特别是在特定突变或肿瘤背景下。针对 TBK1 的抑制剂正在体内和体外环境中开发和应用，但其临床疗效仍然有限。大量文献表明TBK1既具有促肿瘤作用，又具有抑肿瘤作用。 TBK1 作为先天免疫通路中的关键节点，通过激活先天免疫反应来介导抗肿瘤免疫。促进干扰素 I (IFN-I) 的产生是 TBK1 桥接这些过程的关键机制。干扰素已被证明对肿瘤进展既有利又有害。因此，鉴于 TBK1 的下游 IFN-I 信号级联反应，可能需要承认 TBK1 在肿瘤发展中的矛盾作用。在本文中，我们回顾了 TBK1 在各种肿瘤背景下介导的信号通路，并总结了 TBK1 和 TBK1-IFN 通路在促进和抑制肿瘤进展中的双重作用。此外，我们强调了 TBK1-IFN 通路在临床治疗中的重要性，特别是在免疫反应方面。作为新型癌症治疗策略的一部分，我们预计 TBK1 抑制剂的开发将取得进一步进展。版权所有 © 2024 Wang、Zhang、Wu 和 Ji。

TANK-binding kinase 1 (TBK1) is a member of the IKK family and plays a crucial role in the activation of non-canonical NF-κB signaling and type I interferon responses. The aberrant activation of TBK1 contributes to the proliferation and survival of various types of tumor cells, particularly in specific mutational or tumorous contexts. Inhibitors targeting TBK1 are under development and application in both in vivo and in vitro settings, yet their clinical efficacy remains limited. Numerous literatures have shown that TBK1 can exhibit both tumor promoting and tumor inhibiting effects. TBK1 acts as a pivotal node within the innate immune pathway, mediating anti-tumor immunity through the activation of innate immune responses. Facilitating interferon-I (IFN-I) production represents a critical mechanism through which TBK1 bridges these processes. IFN has been shown to exert both beneficial and detrimental effects on tumor progression. Hence, the paradoxical role of TBK1 in tumor development may necessitate acknowledgment in light of its downstream IFN-I signaling cascade. In this paper, we review the signaling pathways mediated by TBK1 in various tumor contexts and summarize the dual roles of TBK1 and the TBK1-IFN pathways in both promoting and inhibiting tumor progression. Additionally, we highlight the significance of the TBK1-IFN pathway in clinical therapy, particularly in the context of immune response. We anticipate further advancements in the development of TBK1 inhibitors as part of novel cancer treatment strategies.Copyright © 2024 Wang, Zhang, Wu and Ji.