Department of Bioscience and Biotechnology, Sejong University, Seoul, Republic of Korea.
Department of Bioscience and Biotechnology, Sejong University, Seoul, Republic of Korea.
Life Sci. 2019 Aug 15;231:116593. doi: 10.1016/j.lfs.2019.116593. Epub 2019 Jun 19.
Inflammasomes are the major mechanistic complexes that include members of the NOD-like receptor (NLRs) or AIM2-like receptors (ALRs) families, which are affiliated with the innate immune system. Once NLRs or ALRs are activated by pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs), the caspase-1 or -11 is activated by binding with NLRs or ALRs via its own unique cytosolic domains. As a result, caspase-1 or -11 enhances the production of IL-1β and IL-18, which results in inflammation via the recruitment of immune cells, such as macrophages, and the promotion of programmed cell death mechanisms such as pyroptosis. In addition, the consistent cascades of inflammasomes would precede both minor and severe autoimmune diseases and cancers. The clinical relevance of inflammasomes in multiple forms of cancer highlights their therapeutic promise as molecular targets. To closely analyze the physiological roles of inflammasomes in cancers, here, we describe the fundamental knowledge regarding the current issues of inflammasomes in relevant cancers, and discuss possible therapeutic values in targeting these inflammasomes for the prevention and treatment of cancer.
炎症小体是主要的机械复合物，包括 NOD 样受体 (NLRs) 或类似的 AIM2 受体 (ALRs) 家族的成员，它们与先天免疫系统有关。一旦 NLRs 或 ALRs 被病原体相关分子模式 (PAMPs) 或损伤相关分子模式 (DAMPs) 激活，caspase-1 或 -11 通过其自身独特的细胞质结构域与 NLRs 或 ALRs 结合而被激活。结果，caspase-1 或 -11 增强了白细胞介素 1β和白细胞介素 18 的产生，从而通过招募巨噬细胞等免疫细胞以及促进细胞程序性死亡机制（如细胞焦亡）导致炎症。此外，炎症小体的一致级联反应会导致轻微和严重的自身免疫性疾病和癌症。炎症小体在多种形式的癌症中的临床相关性突出了它们作为分子靶点的治疗潜力。为了深入分析炎症小体在癌症中的生理作用，在这里，我们描述了与相关癌症中炎症小体的当前问题相关的基础知识，并讨论了针对这些炎症小体进行癌症预防和治疗的可能治疗价值。
