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细菌虫通过LPS介导的TLR4/Myd88/NF-κB通路和炎症变化促进食道状癌的侵袭和转移
Zhongbing Wu1, Jianxin Guo1, Zhenhan Zhang1
1College of Integrated Chinese and Western Medicine, Hebei Medical University, Shijiazhuang, 050017, China.
Scientific reports
|June 4, 2024
概括
细菌菌和它们的脂多糖 (LPS) 促进食道癌症的进展. 这通过炎症和激活TLR4/Myd88/NF-κB通路发生,提供潜在的治疗点.
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:
- 肠道微生物群显著影响胃肠道瘤的发展和食道癌症的进展.
- 驱动食道癌入侵和转移的特定细菌属及其机制尚未完全理解.
研究的目的:
- 研究肠道菌群和代谢物在食道状细胞癌中的作用.
- 阐明特定肠道细菌影响食道癌进展,入侵和转移的机制.
主要方法:
- 对患有食道状细胞癌的患者的肠道菌群和代谢物的分析.
- 在4NQO诱导的小鼠模型中确认食道癌.
- 在体外实验中,使用来自Bacteroides fragilis的脂多糖 (LPS) 对食道癌细胞进行实验.
主要成果:
- 在患者中发现了丰富的细菌体和血脂多糖化物 (LPS) 的增加,与炎症变化相关.
- 在小鼠食道瘤中观察到表皮-介质细胞过渡 (EMT) 和TLR4/Myd88/NF-κB通路激活.
- 来自Bacteroides fragilis的LPS促进了癌细胞的增殖,迁移,入侵,并通过TLR4/Myd88/NF-κB通路激活诱导了EMT.
结论:
- 细菌类物种与食道癌症的进展密切相关.
- 来自Bacteroides的LPS诱导炎症并激活TLR4/Myd88/NF-κB通路,促进癌症的发展.
- 这突出了食道癌预防和治疗的潜在新生物标.
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