PDF(Pubmed)
Abstract：
UNASSIGNED: This study aimed to investigate the effect of selenium on gut microbiota in mice with breast cancer under a high-fat diet.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.
UNASSIGNED: 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.
摘要：
■本研究旨在研究高脂饮食下硒对乳腺癌小鼠肠道菌群的影响。
■将12只雌性BALB/c小鼠随机分为两组:4只T1+硒+高脂饮食组和4只T1+高脂饮食组。小鼠在右侧第4乳腺脂肪垫上注射4个T1细胞，并保持高脂肪饮食。收集粪便样本，提取DNA进行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,探讨高脂饮食状态下硒对乳腺癌的干预作用。
■在高脂肪饮食中补充硒改变了患有乳腺癌的小鼠的肠道微生物群的组成和多样性。硒干预组肠道微生物组成差异显著,随着变形杆菌的丰度增加，放线菌,和Verrucomicrobiaphyla和诸如ganmani螺杆菌之类的物种，日本螺旋杆菌,和阿克曼西亚粘虫，而门，比如拟杆菌,Firmicutes,去铁杆菌,和螺旋藻，和物种,例如普雷沃特拉sp。MGM2，肠壁杆菌，鼠乳杆菌,和普雷沃特拉sp。MGM1，均降低。功能分析揭示了与碳水化合物活性酶相关的基因的差异表达，病原体-宿主相互作用，细胞通讯，细胞自动诱导，膜转运蛋白，和毒力因子。此外，预测了硒干预组中37个COGs和48个代谢潜力上升的代谢物。
■硒改变了高脂饮食乳腺癌小鼠肠道菌群的稳态，影响他们的组成，丰度,和相关的新陈代谢。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焦亡。
■将12只雌性BALB/c小鼠随机分为两组:4只T1+硒+高脂饮食组和4只T1+高脂饮食组。小鼠在右侧第4乳腺脂肪垫上注射4个T1细胞，并保持高脂肪饮食。收集粪便样本，提取DNA进行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,探讨高脂饮食状态下硒对乳腺癌的干预作用。
■在高脂肪饮食中补充硒改变了患有乳腺癌的小鼠的肠道微生物群的组成和多样性。硒干预组肠道微生物组成差异显著,随着变形杆菌的丰度增加，放线菌,和Verrucomicrobiaphyla和诸如ganmani螺杆菌之类的物种，日本螺旋杆菌,和阿克曼西亚粘虫，而门，比如拟杆菌,Firmicutes,去铁杆菌,和螺旋藻，和物种,例如普雷沃特拉sp。MGM2，肠壁杆菌，鼠乳杆菌,和普雷沃特拉sp。MGM1，均降低。功能分析揭示了与碳水化合物活性酶相关的基因的差异表达，病原体-宿主相互作用，细胞通讯，细胞自动诱导，膜转运蛋白，和毒力因子。此外，预测了硒干预组中37个COGs和48个代谢潜力上升的代谢物。
■硒改变了高脂饮食乳腺癌小鼠肠道菌群的稳态，影响他们的组成，丰度,和相关的新陈代谢。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焦亡。
