一种亲致癌的口腔微生物被乳腺癌细胞内化,促进乳腺瘤发生
Sheetal Parida1, Deeptashree Nandi1, Deepak Verma1
1Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Cell communication and signaling : CCS
|January 15, 2026
概括
口腔细菌*F. nucleatum*通过引起炎症和DNA损伤,促进乳腺癌的发展和进展. 由于增强的细菌内部化,BRCA1突变乳腺癌细胞表现出更大的脆弱性.
科学领域:
- 微生物学 微生物学
- 在瘤学瘤学.
- 遗传学 是一个遗传学.
背景情况:
- 肠道微生物组在癌症的发展中起着重要作用.
- 口腔微生物群失调与包括癌症在内的各种系统性疾病有关.
- 口腔细菌在乳腺癌进展中的特定作用尚未完全理解.
研究的目的:
- 为了研究口腔细菌 *F.核菌* 对乳腺癌的致癌影响.
- 探索F.核菌通过哪些机制影响乳腺癌细胞的行为.
- 为了确定 *BRCA1* 突变是否影响乳腺癌细胞对 *F. nucleatum* 的敏感性.
主要方法:
- 乳腺癌组织的基因组分析.
- 哺乳腺殖民实验在小鼠中使用F. nucleatum进行.
- 在体外研究中,暴露乳腺癌细胞 (包括*BRCA1*突变细胞) 于*F. nucleatum*.
主要成果:
- *F.核和相关的口腔微生物在癌症乳腺组织中丰富.
- 在小鼠体内 *F. nucleatum* 的殖民化会引发代塑性病变,炎症,DNA损伤和繁殖.
- *F. nucleatum*在小鼠中加速瘤生长和转移.
- *F. nucleatum*暴露会增加乳腺癌细胞的增殖,迁移,自我更新和化学抵抗.
- *BRCA1* - 突变细胞通过Gal-GalNAc相互作用表现出 *F.核体* 的增强内部化.
结论:
- *F. nucleatum* 作为乳腺癌的致癌驱动因素,影响正常的乳腺上皮,促进瘤的进展.
- 损坏的DNA损伤和修复途径是F. nucleatum瘤原性作用的关键媒介.
- *BRCA1*-突变乳腺癌细胞因细菌吸收增加而优先易受 *F. nucleatum* 的感染.
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