线粒体是在免疫反应过程中产生免疫调节代谢物的信号中枢。此外，线粒体还促进感染期间免疫信号复合物的募集和锚定。 Toll 中的进化保守信号中间体 (ECSIT) 最初被描述为转录因子核因子 kappa-活化 B 细胞轻链增强子 (NF-κB) 的正调节因子。最近，ECSIT 已成为细菌清除、线粒体活性氧 (mROS) 和线粒体自噬的调节剂。此外，ECSIT 已被确定为响应病毒感染和肿瘤发生的控制点。值得注意的是，不同模型和细胞类型中 ECSIT 的缺失被发现会导致肿瘤发生增强。因此，ECSIT 作为代谢肿瘤抑制因子发挥作用并限制癌症发病机制。在这篇综述中，我们重点介绍了 ECSIT 在细胞代谢和免疫之间架起桥梁的关键功能和串扰机制，然后重点关注 ECSIT 独立于免疫的抗肿瘤作用。版权所有 © 2024 Elsevier Ltd。保留所有权利。

Mitochondria are signaling hubs that produce immunomodulatory metabolites during the immune response. In addition, mitochondria also facilitate the recruitment and anchoring of immune signaling complexes during infection. Evolutionary conserved signaling intermediate in toll (ECSIT) was initially described as a positive regulator of the transcription factor Nuclear factor kappa-light chain enhancer of activated B cells (NF-κB). More recently, ECSIT has emerged as a regulator of bacterial clearance, mitochondrial reactive oxygen species (mROS), and mitophagy. In addition, ECSIT has been identified as a control point in responding to viral infection and tumorigenesis. Notably, ECSIT loss in different models and cell types has been found to lead to enhanced tumorigenesis. Thus, ECSIT functions as a metabolic tumor suppressor and limits cancer pathogenesis. In this review, we highlight the key functions and crosstalk mechanisms that ECSIT bridges between cell metabolism and immunity and focus then on the antitumor role of ECSIT independent of immunity.Copyright © 2024 Elsevier Ltd. All rights reserved.