Breast cancer is the most diagnosed malignancy in women. Increasing evidence has highlighted the importance of chronic inflammation at the local and/or systemic level in breast cancer pathobiology, influencing its progression, metastatic potential and therapeutic outcome by altering the tumor immune microenvironment. These processes are mediated by a variety of cytokines, chemokines and growth factors that exert their biological functions either locally or distantly. Inflammasomes are protein signaling complexes that form in response to damage- and pathogen-associated molecular patterns (DAMPS and PAMPS), triggering the release of pro-inflammatory cytokines. The dysregulation of inflammasome activation can lead to the development of inflammatory diseases, neurodegeneration, and cancer. A crucial signaling pathway leading to acute and chronic inflammation occurs through the activation of NLRP3 inflammasome followed by caspase 1-dependent release of IL-1β and IL-18 pro-inflammatory cytokines, as well as, by gasdermin D-mediated pyroptotic cell death. In this review we focus on the role of NLRP3 inflammasome and its components in breast cancer signaling, highlighting that a more detailed understanding of the clinical relevance of these pathways could significantly contribute to the development of novel therapeutic strategies for breast cancer.

中文翻译：

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乳腺癌中NLRP3炎症小体介导的细胞因子产生和焦亡细胞死亡

乳腺癌是女性中诊断最多的恶性肿瘤。越来越多的证据强调了局部和/或全身水平的慢性炎症在乳腺癌病理学中的重要性，通过改变肿瘤免疫微环境影响其进展、转移潜力和治疗结果。这些过程由多种细胞因子、趋化因子和生长因子介导，这些细胞因子、趋化因子和生长因子在局部或远处发挥其生物学功能。炎症小体是蛋白质信号传导复合物，响应损伤和病原体相关分子模式（DAMPS 和 PAMPS）而形成，触发促炎细胞因子的释放。炎症小体激活的失调可导致炎症性疾病、神经退行性变和癌症的发生。导致急性和慢性炎症的关键信号通路是通过激活 NLRP3 炎症小体，然后依赖 caspase 1 释放 IL-1β 和 IL-18 促炎细胞因子，以及gasdermin D 介导的焦亡细胞死亡而发生的。在这篇综述中，我们重点关注 NLRP3 炎性体及其成分在乳腺癌信号传导中的作用，强调更详细地了解这些途径的临床相关性可能会极大地有助于乳腺癌新治疗策略的开发。