Liu Jing, Zhang Yong, Xu Linxiang, Gu Guoli, Dong Zhiwei
Department of General Surgery, Air Force Medical Center, PLA, Beijing, 100142, China.
Department of General Surgery, Air Force Clinical College, China Medical University, Beijing, 100142, China.
J Transl Med. 2025 Jul 2;23(1):734. doi: 10.1186/s12967-025-06675-0.
BACKGROUND: Colorectal cancer (CRC) is the third most prevalent malignant tumor and the second leading cause of cancer-related deaths globally. The genus is an important component of the gut microbiota. and are reported probiotics, and their roles in CRC have been investigated in related studies. However, the association between and CRC remains unknown. METHODS: (10–42) and (22–2) were isolated from healthy human feces. 29 mice that demonstrated normal feeding and activity were randomly assigned to four groups: normal control (NC group), CRC model (IC group), (PJ group), and (LO group). Colonic tumor tissues from the IC, PJ, and LO groups and normal colon tissues from the NC group were then collected for HE staining and immunohistochemical staining. Fecal samples from mice during the hyperproliferative and adenoma phases were collected for Metagenomic sequencing and metabolite analysis. RESULTS: intervention reduced the number and slowed the growth of colonic tumors, improved tumor histological scores, and decreased microenvironmental inflammation levels. improved the composition of intestinal flora in mice with colon cancer, increased gut microbial species diversity, and maintained gut microbiota stability. Furthermore, intervention increased the abundance of and , which play a role in ameliorating AOM/DSS-induced gut microbiota dysbiosis. intervention affected the metabolic pathways, including amino sugar degradation and galactose metabolism, sphingolipid synthesis, amino acid synthesis, and polyphenol synthesis pathways, with the tryptophan metabolism pathway as the primary pathway being affected. CONCLUSION: Our study profiled the administration reduces the number of tumors and lower tumor staging in AOM/DSS-induced colon cancer mice by modulating gut microbiota and its metabolites at early stages. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12967-025-06675-0.
背景:结直肠癌(CRC)是全球第三大常见恶性肿瘤,也是癌症相关死亡的第二大主要原因。[此处原文缺失具体微生物属名称]属是肠道微生物群的重要组成部分。[此处原文缺失具体微生物名称]和[此处原文缺失具体微生物名称]是已报道的益生菌,其在结直肠癌中的作用已在相关研究中进行了调查。然而,[此处原文缺失具体微生物名称]与结直肠癌之间的关联仍然未知。 方法:从健康人粪便中分离出[此处原文缺失具体微生物名称](10 - 42)和[此处原文缺失具体微生物名称](22 - 2)。将29只表现出正常进食和活动的小鼠随机分为四组:正常对照组(NC组)、结直肠癌模型组(IC组)、[此处原文缺失具体微生物名称]组(PJ组)和[此处原文缺失具体微生物名称]组(LO组)。然后收集IC组、PJ组和LO组的结肠肿瘤组织以及NC组的正常结肠组织进行苏木精 - 伊红(HE)染色和免疫组织化学染色。收集小鼠在增生和腺瘤阶段的粪便样本进行宏基因组测序和代谢物分析。 结果:[此处原文缺失具体微生物名称]干预减少了结肠肿瘤的数量并减缓了其生长,改善了肿瘤组织学评分,并降低了微环境炎症水平。[此处原文缺失具体微生物名称]改善了结肠癌小鼠的肠道菌群组成,增加了肠道微生物物种多样性,并维持了肠道微生物群的稳定性。此外,[此处原文缺失具体微生物名称]干预增加了[此处原文缺失具体微生物名称]和[此处原文缺失具体微生物名称]的丰度,它们在改善氧化偶氮甲烷/葡聚糖硫酸钠(AOM/DSS)诱导的肠道微生物群失调中发挥作用。[此处原文缺失具体微生物名称]干预影响了代谢途径,包括氨基糖降解和半乳糖代谢、鞘脂合成、氨基酸合成以及多酚合成途径,其中色氨酸代谢途径是受影响的主要途径。 结论:我们的研究表明,[此处原文缺失具体微生物名称]给药通过在早期调节肠道微生物群及其代谢物,减少了AOM/DSS诱导的结肠癌小鼠的肿瘤数量并降低了肿瘤分期。 补充信息:在线版本包含可在10.1186/s12967 - 025 - 06675 - 0获取的补充材料。
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