性饮食在触发瘤转移中发挥了意想不到的作用,因为它通过调节BACH1-介导的转录来触发瘤转移
Zhenyi Su1,2, Yanqing Liu1,2, Zhangchuan Xia1,2
1Institute for Cancer Genetics, and Department of Pathology and Cell Biology, Vagelos College of Physicians and Surgeons, Columbia University, 1130 Nicholas Ave, New York, NY 10032, USA.
Science advances
|June 5, 2024
概括
性 (Keto) 饮食意外地促进了小鼠的癌症转移,通过调节BACH1. 抑制BACH1或ATF4会阻断这种效应,这表明癌症患者存在潜在风险.
科学领域:
- 在瘤学瘤学.
- 分子生物学分子生物学
- 代谢过程中的代谢.
背景情况:
- 素 (Keto) 饮食在体重管理和某些健康状况方面越来越受欢迎.
- 新兴研究表明饮食在癌症进展中的潜在作用,但机制往往不清楚.
研究的目的:
- 研究凯托饮食对癌细胞转移潜力的影响.
- 阐明导致饮食引起的瘤转移的分子机制.
主要方法:
- 利用互补的小鼠模型来研究瘤转移.
- 研究了BTB域和CNC同源1 (BACH1) 和激活转录因子4 (ATF4) 在饮食诱导的转移中的作用.
- 采用了基因淘汰和药物抑制策略.
主要成果:
- 凯托饮食在小鼠模型中显著促进了癌细胞转移.
- 基托饮食诱导的转移依赖于BACH1的上调调节及其前转移性标,例如诱导细胞迁移的氨酶1.
- 对BACH1的遗传或药理抑制消除了Keto饮食的转移性影响.
- 凯托饮食诱导了激活转录因子4 (ATF4),它与BACH1相互作用,增强了前转移基因的转录.
结论:
- 涉及BACH1的独特的转录调节程序调解了Keto饮食诱导的瘤转移.
- 这些发现表明,对于癌症患者而言,Keto饮食存在潜在的健康风险.
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