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细菌的脂多糖化物改变了结直肠癌细胞中的DNA甲基化

Jessica Permain¹, Arielle Sulit¹, Timothy Eglinton¹

¹Department of Surgery and Critical Care, University of Otago, Christchurch, Aotearoa, New Zealand.

Clinical epigenetics

|December 6, 2025

概括

来自Fusobacterium periodonticum和Bacteroides fragilis的细菌脂多糖 (LPS) 改变了结直肠癌细胞中的DNA甲基化. 这表明细菌可能通过表观遗传修饰影响结直肠癌的发展.

科学领域:

表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
微生物学微生物学
在瘤学瘤学.

背景情况:

大肠直肠癌 (CRC) 与诸如DNA甲基化等表观遗传变化有关.
瘤寄存细菌与CRC有关,但它们的表观遗传影响尚不清楚.
在高CpG岛甲基化表型 (CIMP) 的CRC瘤中,Fusobacterium periodonticum和Bacteroides fragilis是常见的.

研究的目的:

研究F. periodonticum和B. fragilis中的脂多糖 (LPS) 对结直肠癌细胞中DNA甲基化的影响.
探索细菌LPS如何影响CRC中的基因表达.
建立肠道细菌与结直肠癌中的表观遗传调节之间的联系.

主要方法:

在HT29结直肠癌细胞中,使用来自F. periodonticum和B. fragilis的LPS进行了治疗.
减少表示双硫酸盐测序 (RRBS) 用于评估DNA甲基化.
RT-qPCR分析了与改变的DNA甲基化相关的基因表达变化.

主要成果:

F. periodonticum LPS诱导了高甲基化和低甲基化,影响了PEPD和VAV3基因促进物甲基化,并降低了它们的表达.
B. fragilis LPS主要导致低甲基化.
联合LPS治疗显示出不同的模式,其中B. fragilis LPS部分减少了F. periodonticum LPS诱导的高甲基化.

结论:

细菌LPS可以动态地改变结直肠癌细胞中的DNA甲基化概况,影响基因表达.
这项研究揭示了瘤寄存细菌与CRC中的DNA甲基化之间的新鲜联系.
这些发现表明,细菌通过表观遗传修饰对结直肠癌发生产生潜在影响机制.

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