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由肠道微生物衍生的N-乙慕拉胺酸通过AKT1通路减轻结直肠癌

Mengyao Hu¹, Yi Xu¹, Yuqing Wang¹

¹Microbiome Medicine Center, Department of Laboratory Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, China.

|February 27, 2025

概括

作为肠道微生物代谢物N-乙木氨酸 (NAM) 通过向AKT1通路来抑制结直肠癌 (CRC) 的发展. 这一发现表明NAM.

科学领域:

微生物学和瘤学
肠道微生物组研究研究
癌症生物学癌症生物学

背景情况:

肠道微生物代谢物极大地影响着结直肠癌 (CRC) 的发展.
糖片段 (PGF) 是影响肠道平衡的关键微生物产物,但它们在CRC中的作用尚不清楚.

研究的目的:

调查PGFs在肠道瘤发生中的潜在作用.
探索PGFs作为CRC的潜在生物标志物.

主要方法:

在CRC患者中对酸甘合成和降解基因的元基因组学分析.
在患者样本中使用向质谱学量化特定的PGFs.
在体内和体外评估PGF对结直肠瘤生长的影响,使用小鼠模型和患者衍生器官.
涉及蛋白质组和转录组分析的机制研究,以确定分子标.

主要成果:

在7个队列 (n=1121) 中,在CRC患者中观察到减少糖甘合成基因的丰度.
在CRC患者中发现的一种特定PGFN-乙慕拉胺酸 (NAM) 的显著耗尽,随着瘤的进展而减少.
在多个临床前模型中,NAM证明了肠道瘤发生的显著抑制,并减少了CRC有机体的生长.
发现NAM通过直接结合和阻断酸化来抑制AKT1的激活,部分介导其抗癌作用.

结论:

通过向AKT1信号通路,N-乙慕拉胺酸 (NAM) 对肠道瘤发生具有保护作用.
作为结直肠癌 (CRC) 的新型预防和治疗生物标志物,NAM显示出希望.

关键词:

结肠中的微生物群结肠癌是一种大肠癌.

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