本研究旨在探讨硒对高脂饮食下乳腺癌小鼠肠道菌群的影响。 共12只雌性BALB/c小鼠随机分为两组：4 T1  硒高脂饮食组和4 T1  高脂饮食组。小鼠在右侧第四乳腺脂肪垫注射了 4 T1 细胞，并保持高脂肪饮食。收集粪便样本，提取DNA用于宏基因组测序和生物信息学分析。对相关靶基因和通路进行注释和代谢分析，探讨硒对高脂饮食状态下乳腺癌的干预作用。高脂饮食中补硒改变了乳腺癌小鼠肠道菌群的组成和多样性。硒干预组的肠道微生物组成显着不同，变形菌门、放线菌门和疣微菌门以及甘马尼螺杆菌、日本螺杆菌和嗜粘蛋白阿克曼氏菌等物种丰度增加，而拟杆菌门、厚壁菌门、去铁杆菌门等菌门丰度增加。和螺旋体，以及物种，例如普雷沃氏菌属。 MGM2、肠鼠杆菌、鼠乳杆菌和普雷沃菌属。 MGM1 减少。功能分析揭示了与碳水化合物活性酶、病原体-宿主相互作用、细胞通讯、细胞自诱导、膜转运蛋白和毒力因子相关的基因的差异表达。此外，还预测了硒干预组中 37 种 COG 和 48 种代谢潜力上升的代谢物。硒改变了高脂肪饮食的乳腺癌小鼠肠道微生物群的稳态，影响其组成、丰度和相关代谢。这些发现表明，该机制涉及干扰肠道微生物群稳态，导致肿瘤相关蛋白质和脂肪酸的合成改变，并诱导肿瘤细胞凋亡和细胞焦亡。版权所有 © 2024 Li、Liu、Kong、Zhang 和 Zhu。

This study aimed to investigate the effect of selenium on gut microbiota in mice with breast cancer under a high-fat diet.A total of 12 female BALB/c mice were randomly divided into two groups: 4 T1 + selenium+ high-fat diet group and 4 T1 + high-fat diet group. Mice were injected with 4 T1 cells on the right 4th mammary fat pad and kept on a high-fat diet. Fecal samples were collected, and DNA was extracted for metagenomic sequencing and bioinformatics analysis. Relevant target genes and pathways were annotated and metabolically analyzed to explore the intervention effect of selenium on breast cancer in the high-fat diet state.Selenium supplementation in the high-fat diet altered the composition and diversity of gut microbiota in mice with breast cancer. The gut microbial composition was significantly different in the selenium intervention group, with an increased abundance of Proteobacteria, Actinobacteria, and Verrucomicrobia phyla and species such as Helicobacter ganmani, Helicobacter japonicus, and Akkermansia muciniphila, while phyla, such as Bacteroidetes, Firmicutes, Deferribacteres, and Spirochaetes, and species, such as Prevotella sp. MGM2, Muribaculum intestinale, Lactobacillus murinus, and Prevotella sp. MGM1, were decreased. Functional analysis revealed differential expression of genes related to carbohydrate-active enzymes, pathogen-host interactions, cell communication, cell auto-induction, membrane transporters, and virulence factors. Furthermore, 37 COGs and 48 metabolites with rising metabolic potential in the selenium intervention group were predicted.Selenium alters the homeostasis of gut microbiota in mice with breast cancer on a high-fat diet, affecting their composition, abundance, and associated metabolism. These findings suggest that the mechanism involves interfering with gut microbiota homeostasis, leading to altered synthesis of tumor-associated proteins and fatty acids and inducing tumor cell apoptosis and pyroptosis.Copyright © 2024 Li, Liu, Kong, Zhang and Zhang.