乙酸重新编程瘤新陈代谢,并通过上调c-Mycc来促进PD-L1表达和免疫逃避
Juhong Wang1,2, Yannan Yang1,2, Fei Shao1,2,3
1Department of Thoracic Surgery, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Nature metabolism
|May 3, 2024
概括
乙酸通过重编程新陈代谢和促进免疫逃避来促进非小细胞肺癌的生长. 向酸盐摄取可能会提高抗PD-1疗法的疗效.
科学领域:
- 生物化学 生物化学
- 在瘤学瘤学.
- 免疫学 免疫学 免疫学
背景情况:
- 乙酸是乙-CoA的关键代谢前体,对于细胞过程至关重要.
- 酸在重编程瘤代谢和免疫逃避中的作用尚不清楚.
研究的目的:
- 调查乙酸在非小细胞肺癌 (NSCLC) 代谢和免疫逃避中的作用.
- 探索针对NSCLC中酸盐代谢的治疗潜力.
主要方法:
- 对人类NSCLC组织中酸盐水平和吸收的分析.
- 研究乙酸盐诱导的c-Myc乙化机制.
- 评估饮食中酸盐和酸盐摄取中断对瘤生长,免疫细胞透和体内抗PD-1治疗反应的影响.
主要成果:
- 乙酸是NSCLC中最丰富的短链脂肪酸,瘤吸收增加.
- 乙酸盐促进c-Myc乙化,增强其稳定性,并对参与免疫逃避 (PD-L1),糖分解和细胞循环的基因进行上调.
- 食中酸盐补充剂加速瘤生长,并减少CD8+ T细胞的透.
- 干扰乙酸的吸收抑制免疫逃避,并提高抗PD-1疗法的疗效.
结论:
- 乙酸通过重编程瘤代谢来促进NSCLC的生长和免疫逃避.
- 向乙酸代谢是提高抗PD-1免疫治疗结果的潜在策略.
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