文章：

分化炎性体信号在肿瘤发生和潜在靶向中的作用

Diverging inflammasome signals in tumorigenesis and potential targeting

原文发布日期：2019-03-06

DOI: 10.1038/s41568-019-0123-y

类型: Review Article

开放获取: 否

英文摘要：

Inflammasomes are molecular platforms that assemble upon sensing various intracellular stimuli. Inflammasome assembly leads to activation of caspase 1, thereby promoting the secretion of bioactive interleukin-1β (IL-1β) and IL-18 and inducing an inflammatory cell death called pyroptosis. Effectors of the inflammasome efficiently drive an immune response, primarily providing protection against microbial infections and mediating control over sterile insults. However, aberrant inflammasome signalling is associated with pathogenesis of inflammatory and metabolic diseases, neurodegeneration and malignancies. Chronic inflammation perpetuated by inflammasome activation plays a central role in all stages of tumorigenesis, including immunosuppression, proliferation, angiogenesis and metastasis. Conversely, inflammasome signalling also contributes to tumour suppression by maintaining intestinal barrier integrity, which portrays the diverse roles of inflammasomes in tumorigenesis. Studies have underscored the importance of environmental factors, such as diet and gut microbiota, in inflammasome signalling, which in turn influences tumorigenesis. In this Review, we deliver an overview of the interplay between inflammasomes and tumorigenesis and discuss their potential as therapeutic targets.

摘要翻译： 

炎症小体是感知各种细胞内刺激后组装形成的分子平台。其组装会激活caspase-1，进而促进生物活性白细胞介素-1β（IL-1β）和IL-18的分泌，并诱导称为焦亡的炎症性细胞死亡。炎症小体效应物能有效驱动免疫应答，主要提供抗微生物感染保护并介导对无菌损伤的控制。然而，异常的炎症小体信号传导与炎症代谢性疾病、神经退行性病变及恶性肿瘤的发病机制相关。由炎症小体激活延续的慢性炎症在肿瘤发生的所有阶段（包括免疫抑制、增殖、血管生成和转移）均发挥核心作用。相反，炎症小体信号通过维持肠道屏障完整性也有助于肿瘤抑制，这揭示了炎症小体在肿瘤发生中的双重作用。研究强调了饮食和肠道微生物组等环境因素在炎症小体信号传导中的重要性，而该信号传导又会影响肿瘤发生。本文综述将阐述炎症小体与肿瘤发生之间的相互作用，并探讨其作为治疗靶点的潜力。

原文链接：

Diverging inflammasome signals in tumorigenesis and potential targeting