乳腺癌（BC）是女性生殖系统的一种常见癌症，也是癌症相关死亡率的主要原因。 NLRP3 是一种关键的炎症小体，其激活与肿瘤相关的分子和细胞过程广泛相关。然而，NLRP3在乳腺癌中的调节机制和具体作用仍未完全阐明。本研究旨在评估 BC 中 NLRP3 相关基因的分子机制。本研究利用生物信息学方法对TCGA-BRCA数据集进行了分析，其中包括正常（WT）、NLRP3敲除（KO）、非敲除-BRCA（BC-WT）和NLRP3-四组转录组测序数据。敲除-BRCA (BC-KO)。结果表明，NLRP3 在 TCGA-BRCA 中显着下调。关键模块基因主要富集于白细胞、细胞间粘附和细胞因子-细胞因子受体相互作用。此外，相关性分析显示NLRP3与癌症相关成纤维细胞呈正相关，与CD4 Th1 T细胞呈负相关。此外，DEGs1和DEGs2重叠表明有505个特征基因，其中Chac1（阴性）和Ugt8a（阳性）与差异免疫细胞（类别转换记忆B细胞）的相关性最强。通路交叉揭示了 13 条 co-KEGG 通路。 BC-KO组表明四种基因（Ccl19、Ccl20、Ccl21a和H2-Oa）的水平显着降低，两种基因（Il2ra和H2-Ob）的水平升高。本研究深入探讨了NLRP3在BC中的作用，探讨其调控机制和影响基因敲除。生物信息学方法鉴定了 NLRP3 相关基因、其丰富的通路以及肿瘤微环境 (TME) 内的相互作用，为 NLRP3 功能、TME 动态以及 BC 预防和治疗的潜在靶点提供了新的见解。版权所有 © 2024 作者。由爱思唯尔公司出版。保留所有权利。

Breast cancer (BC) is a prevalent cancer of the female reproductive system and a major contributor to cancer-related mortality. The activation of NLRP3, a key inflammasome, has been extensively associated with tumor-related molecular and cellular processes; however, the regulatory mechanisms and specific role of NLRP3 in breast cancer remain incompletely elucidated. This study aimed to evaluate the molecular mechanisms of NLRP3-related genes in BC. Utilizing bioinformatics methods, the present research analyzed the TCGA-BRCA dataset, which included four groups of transcriptome sequencing data as follows, normal (WT), NLRP3 knockout (KO), non-knockout-BRCA (BC-WT), and NLRP3-knockout-BRCA (BC-KO). Results indicated that NLRP3 was significantly down-regulated in TCGA-BRCA. Key module genes were mainly enriched in leukocyte cell-cell adhesion and cytokine-cytokine receptor interaction. Moreover, correlation analysis showed that NLRP3 was positively associated with cancer-associated fibroblasts and negatively associated with CD4+ Th1 T-cells. In addition, the DEGs1 and DEGs2 overlapping indicated 505 feature genes, with Chac1 (negative) and Ugt8a (positive) had the strongest correlation with differential immune cells (class-switched memory B cells). Pathway intersection revealed 13 co-KEGG pathways. The BC-KO group indicated markedly reduced levels of four genes (Ccl19, Ccl20, Ccl21a, and H2-Oa) and increased levels of two genes (Il2ra and H2-Ob). This study delved into the role of NLRP3 in BC, exploring its regulatory mechanisms and the impact gene knockout. Bioinformatics approaches identified NLRP3-associated genes, their enriched pathways, and interactions within the tumor microenvironment (TME), providing novel insights into NLRP3 function, TME dynamics, and potential targets for BC prevention and treatment.Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.