Catenibacteriummitsuokai通过与肝细胞结合并产生林酸来促进肝细胞致癌
Ying Zhang1, Weixin Liu2, Chi Chun Wong2
1Department of Oncology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China; Department of Medicine and Therapeutics, Institute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong SAR, China.
Cell metabolism
|September 26, 2025
概括
肠道细菌Catenibacterium mitsuokai通过破坏肠道屏障和殖民肝脏来促进肝癌 (HCC). 它的代谢物林酸激活了TIE2通路,推动了HCC的进展.
科学领域:
- 微生物学 微生物学
- 在瘤学瘤学.
- 胃肠病学 胃肠病学
背景情况:
- 肠道微生物群在肝细胞癌 (HCC) 发病过程中的作用尚未完全理解.
- 鉴定参与HCC发展的特定肠道细菌对于了解疾病机制至关重要.
研究的目的:
- 研究Catenibacterium mitsuokai在HCC发育中的作用.
- 阐明C.mitsuokai促进HCC的分子机制.
主要方法:
- 分析来自HCC患者的便和瘤样本.
- 使用常规和无菌小鼠模型进行体内研究.
- 研究细菌转移,蛋白质-连接体相互作用和代谢物驱动的信号通路.
主要成果:
- 在HCC患者的便和瘤中,Catenibacterium被丰富.
- 在小鼠中,C. mitsuokai加速了HCC,破坏了肠道屏障,并转移到肝脏.
- 在C. mitsuokai的蛋白质Gtr1/RagA通过与HCC细胞上的γ-catenin相互作用来调解肝脏殖民.
- 代谢物林酸激活了HCC细胞上的TIE2受体,导致PI3K/AKT通路激活和HCC进展.
结论:
- Catenibacterium mitsuokai是一种新的肠道细菌,涉及HCC的病变发生.
- C.mitsuokai通过破坏肠道屏障,殖民肝脏,并通过林酸激活TIE2/PI3K/AKT信号通路来促进HCC.
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