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炎症小体对癌症的调控:从炎症到肿瘤发生

Regulation of cancer by inflammasomes: from inflammation to tumorigenesis.

作者信息

Malvankar Shivani, Jaiswal Pundrik, Bhat Panchami P, Mehto Subhash

机构信息

Immunobiology Laboratory, Department of Biosciences and Bioengineering, Indian Institute of Technology, Dharwad, Karnataka, India.

Laboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, The National Institutes of Health, Bethesda, MD, United States.

出版信息

Front Immunol. 2025 Jul 7;16:1611719. doi: 10.3389/fimmu.2025.1611719. eCollection 2025.

DOI:10.3389/fimmu.2025.1611719
PMID:40692785
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12277140/
Abstract

Inflammation is closely linked to the development and progression of cancer, as well as the effectiveness of cancer treatment. Inflammation is an immune response triggered when the immune system detects harmful stimuli such as pathogens, damaged cells, or toxic substances through pattern recognition receptors (PRRs). This activates signaling pathways and inflammasomes leading to the release of pro-inflammatory cytokines. In chronic inflammation, immune cells such as T and B lymphocytes, play a significant role in amplifying and sustaining the inflammatory response. The Inflammasomes are protein complexes that respond to microbes and danger signals, triggering an inflammatory response. Key inflammasomes, including NLRP3, AIM2, and NLRC4, regulate the release of proinflammatory cytokines and induce pyroptosis. While inflammasome activation is vital for immune defense, its dysregulation is associated with various diseases, including cancer. The relationship between inflammasomes and cancer is complex and varies depending on the context, with studies showing both promotion and inhibition of tumor growth. This review highlights the connection between microbes and radiation induced inflammatory regulators and cancer, stressing the need for research to understand the mechanisms through which inflammasomes and other inflammatory sensors control cancer.

摘要

炎症与癌症的发生、发展以及癌症治疗的效果密切相关。炎症是免疫系统通过模式识别受体(PRR)检测到病原体、受损细胞或有毒物质等有害刺激时触发的免疫反应。这会激活信号通路和炎性小体,导致促炎细胞因子的释放。在慢性炎症中,T淋巴细胞和B淋巴细胞等免疫细胞在放大和维持炎症反应中起重要作用。炎性小体是对微生物和危险信号作出反应、触发炎症反应的蛋白质复合物。包括NLRP3、AIM2和NLRC4在内的关键炎性小体调节促炎细胞因子的释放并诱导细胞焦亡。虽然炎性小体激活对免疫防御至关重要,但其失调与包括癌症在内的各种疾病有关。炎性小体与癌症之间的关系复杂,因情况而异,研究表明其对肿瘤生长既有促进作用也有抑制作用。本综述强调了微生物和辐射诱导的炎症调节因子与癌症之间的联系,强调需要开展研究以了解炎性小体和其他炎症传感器控制癌症的机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8752/12277140/f5d71a2ed4e5/fimmu-16-1611719-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8752/12277140/f5d71a2ed4e5/fimmu-16-1611719-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8752/12277140/f5d71a2ed4e5/fimmu-16-1611719-g001.jpg

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本文引用的文献

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Role of the AIM2 Inflammasome in Cancer: Potential Therapeutic Strategies.AIM2炎性小体在癌症中的作用:潜在治疗策略
Biomedicines. 2025 Feb 6;13(2):395. doi: 10.3390/biomedicines13020395.
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The role of AIM2 in inflammation and tumors.AIM2 在炎症和肿瘤中的作用。
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AIM2 promotes irradiation resistance, migration ability and PD-L1 expression through STAT1/NF-κB activation in oral squamous cell carcinoma.AIM2 通过激活 STAT1/NF-κB 促进口腔鳞状细胞癌的辐射抗性、迁移能力和 PD-L1 表达。
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NLRP3 inflammasome activation in sensory neurons promotes chronic inflammatory and osteoarthritis pain.感觉神经元中的NLRP3炎性小体激活会促进慢性炎症和骨关节炎疼痛。
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NLRP3 Inhibition Leads to Impaired Mucosal Fibroblast Function in Patients with Inflammatory Bowel Diseases.NLRP3 抑制导致炎症性肠病患者黏膜成纤维细胞功能受损。
J Crohns Colitis. 2024 Mar 1;18(3):446-461. doi: 10.1093/ecco-jcc/jjad164.
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Expression and clinical value of NLRP1 and NLRC4 inflammasomes in prostate cancer.NLRP1和NLRC4炎性小体在前列腺癌中的表达及临床价值
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Aberrant inflammasome activation as a driving force of human autoimmune skin disease.异常的炎性体激活作为人类自身免疫性皮肤病的驱动因素。
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