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Diverging inflammasome signals in tumorigenesis and potential targeting.
Nature Reviews Cancer ( IF 72.5 ) Pub Date : 2019-04-01 , DOI: 10.1038/s41568-019-0123-y
Rajendra Karki 1 , Thirumala-Devi Kanneganti 1
Nature Reviews Cancer ( IF 72.5 ) Pub Date : 2019-04-01 , DOI: 10.1038/s41568-019-0123-y
Rajendra Karki 1 , Thirumala-Devi Kanneganti 1
Affiliation
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.
中文翻译:
在肿瘤发生和潜在靶向中发炎的信号有所不同。
炎性小体是在感知各种细胞内刺激后组装的分子平台。炎症小体组装导致caspase 1的活化,从而促进生物活性白介素1β(IL-1β)和IL-18的分泌,并引起称为烧伤的炎性细胞死亡。炎性小体的效应子有效地驱动了免疫反应,主要为抵抗微生物感染提供了保护并介导了对无菌损伤的控制。然而,异常的炎性体信号传导与炎性和代谢性疾病,神经变性和恶性肿瘤的发病机理有关。炎性体激活导致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)起着核心作用。反过来,炎性体信号传导还通过维持肠屏障完整性来促进肿瘤抑制,这反映了炎性体在肿瘤发生中的不同作用。研究已经强调了环境因素(如饮食和肠道菌群)在炎症小体信号传导中的重要性,而这些反过来又会影响肿瘤的发生。在本综述中,我们概述了炎症小体与肿瘤发生之间的相互作用,并讨论了它们作为治疗靶标的潜力。
更新日期:2019-07-05
中文翻译:
在肿瘤发生和潜在靶向中发炎的信号有所不同。
炎性小体是在感知各种细胞内刺激后组装的分子平台。炎症小体组装导致caspase 1的活化,从而促进生物活性白介素1β(IL-1β)和IL-18的分泌,并引起称为烧伤的炎性细胞死亡。炎性小体的效应子有效地驱动了免疫反应,主要为抵抗微生物感染提供了保护并介导了对无菌损伤的控制。然而,异常的炎性体信号传导与炎性和代谢性疾病,神经变性和恶性肿瘤的发病机理有关。炎性体激活导致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)起着核心作用。反过来,炎性体信号传导还通过维持肠屏障完整性来促进肿瘤抑制,这反映了炎性体在肿瘤发生中的不同作用。研究已经强调了环境因素(如饮食和肠道菌群)在炎症小体信号传导中的重要性,而这些反过来又会影响肿瘤的发生。在本综述中,我们概述了炎症小体与肿瘤发生之间的相互作用,并讨论了它们作为治疗靶标的潜力。