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Updated: Jul 7, 2026

In vitro Organoid Culture of Primary Mouse Colon Tumors
Published on: May 17, 2013
抗万科胺素耐药的Enterococcus faecalis对结肠癌细胞的致病性
Li Zhang1, Mingxia Deng2, Jing Liu2
1Department of Gastroenterology and Hepatology, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, Jiangsu, China.
耐万科素的菌 (Enterococcus faecalis) 促进血管生成,并激活结肠细胞中的PI3K/AKT/mTOR通路. 这些行动表明VREs有助于结直肠癌 (CRC) 的发展.
科学领域:
- 微生物学 微生物学
- 细胞生物学 细胞生物学
- 在瘤学瘤学.
背景情况:
- 在人类结肠细胞中研究抗万科素的病原性Enterococcus faecalis (VREs).
- 了解VREs在抗生素耐药性和潜在疾病发展的背景下的作用.
研究的目的:
- 评估VREs在人结肠细胞系上的体外致病性.
- 确定VREs对血管生成和关键细胞信号通路的影响.
- 为了将VREs的影响与标准Enterococcus faecalis菌株进行比较.
主要方法:
- 与人类结肠细胞系 (NCM460,HT-29,HCT116) 共同培养的E. faecalis分离物 (VREs和ATCC 29212) 和人类结肠细胞系.
- 对细菌粘附的评估,细胞形态,IL-8和VEGFA表达 (RT-qPCR,ELISA).
- 血管新生试验 (细胞迁移,HUVEC管形成) 和PI3K/AKT/mTOR通路分析 (西部斑点).
主要成果:
- E. faecalis 的生长和粘附依赖于MOI.
- 与标准菌株相比,VREs对NCM460和HT-29细胞的侵袭作用较小.
- E. faecalis,特别是VREs,通过IL-8和VEGFA分泌促进了血管生成,并激活了PI3K/AKT/mTOR通路.
结论:
- VREs促进血管生成,并激活结肠细胞中的PI3K/AKT/mTOR信号通路.
- 这些机制表明VREs在结直肠癌 (CRC) 的发生和发展中发挥了作用.
- 对VREs在CRC病原发生中的作用进行进一步研究是有必要的.
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