缺乏eIF6可以通过调节肠道微生物群和相关代谢物来缓解结直肠癌
Shuai Yang1, Jiawei Song1, Zhenzhen Wang2
1Comprehensive Laboratory for Biology Teaching, College of Life Sciences, Xuzhou Medical University, Xuzhou, Jiangsu, China.
Cell death and differentiation
|January 31, 2026
概括
缺乏eIF6可以通过促进有益的肠道细菌来预防结直肠癌 (CRC). 这导致印-3-碳酸 (3-ICA) 的产生增加,这种化合物抑制瘤生长并增强肠道屏障功能.
科学领域:
- 在瘤学瘤学.
- 微生物学 微生物学
- 分子生物学分子生物学
背景情况:
- 过度表达eIF6在各种癌症中很常见.
- 已知eIF6缺乏会改变肠道微生物群的组成.
- 需要进一步调查eIF6,肠道失调和结直肠癌 (CRC) 之间的相互作用.
研究的目的:
- 阐明连接eIF6缺乏,微生物失调和结直肠癌 (CRC) 的机制.
- 评估针对CRC中的eIF6-微生物群轴的治疗潜力.
主要方法:
- 在人类和小鼠CRC样本中评估eIF6表达.
- 利用AOM/DSS诱导的CRC小鼠模型与抗生素治疗和便微生物群移植 (FMT).
- 采用了16S rDNA测序,Dubosiella newyorkensis (D. newyorkensis) 补充剂,以及代谢物分析 (3-ICA).
主要成果:
- 在小鼠中,eIF6缺乏减少了CRC发生率和瘤增殖.
- 缺乏eIF6会增加有益细菌 (Akkermansia, Dubosiella) 和改善肠道屏障功能.
- 从eIF6缺乏的小鼠和D. newyorkensis中获得的FMT减轻了CRC;3-ICA抑制了CRC的进展.
结论:
- 通过丰富D. newyorkensis及其代谢物3-ICA. 的蛋白质,eIF6缺乏能提供对CRC的保护.
- 这项研究揭示了一种涉及肠道微生物群在CRC发展中的新机制.
- 针对eIF6-微生物群-代谢物轴为CRC提供了潜在的治疗策略.
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