细菌,肺癌组织和巨细胞之间的DC-SIGN (CD209) 中介相互作用促进癌症转移
Qiao Li1, Nihal Hasan1, Fei Zhao1
1Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology, Wuhan, Hubei, China.
Infectious agents and cancer
|June 21, 2025
概括
细菌感染,特别是Shigella sonnei,可能通过劫持免疫细胞上的DC-SIGN受体来促进肺癌转移. 这种相互作用增强了癌细胞的迁移和瘤的生长,突出了癌症进展的新机制.
科学领域:
- 在瘤学瘤学.
- 微生物学 微生物学
- 免疫学 免疫学 免疫学
背景情况:
- 肺癌转移包括癌细胞的扩散.
- 细菌感染越来越多地与癌症的发展和转移有关.
- 阴性细菌利用抗原呈现细胞 (APC) 上的DC-SIGN受体来促进病原体的传播.
研究的目的:
- 通过DC-SIGN调查细菌感染促进肺癌细胞通过DC-SIGN传播的假设.
- 探索将细菌感染与肺癌转移联系在一起的分子机制.
主要方法:
- 在人类肺癌组织中分析细菌DNA多样性.
- 对肺癌组织中DC-SIGN表达的评估及其与Shigella sonnei的相互作用.
- 关于巨细胞DC-SIGN诱导和癌细胞迁移的体外研究.
- 在体内实验中使用感染了Shigella sonnei.的野生类型和SIGNR1淘汰赛小鼠进行实验.
主要成果:
- 人类肺癌组织表现出高的细菌DNA多样性.
- 肺癌组织表达DC-SIGN,促进与Shigella sonnei结合.
- 石格拉·索尼 (Shigella sonnei) 在巨细胞上诱导DC-SIGN表达,并在体外增强肺癌细胞迁移.
- 在野外型小鼠中,Shigella sonnei感染显著增加了瘤大小,重量和转移,与淘汰小鼠相比,与DC-SIGN表达相关.
结论:
- 细菌感染,以Shigella sonnei为例,可以促进肺癌的进展和转移.
- DC-SIGN受体在调解细菌感染对肺癌转移的影响方面发挥着至关重要的作用.
- 针对DC-SIGN介导机制可能为肺癌提供新的治疗策略.
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