巨细胞在TME中"感知"肥胖驱动的酸性
Spenser H Stone1, Jeffrey C Rathmell2, Jackie E Bader1
1Department of Pathology Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, TN, USA.
Cell chemical biology
|December 20, 2024
概括
肥胖通过改变瘤微环境来促进癌症. 由于酸性,与瘤相关的巨细胞因酸性而提高GPR65的调节,损害其功能并促进瘤生长.
科学领域:
- 免疫学 免疫学 免疫学
- 在瘤学瘤学.
- 代谢综合征是代谢综合征的一种.
背景情况:
- 肥胖是许多癌症的重要风险因素和预后指标.
- 瘤微环境在癌症进展中起着至关重要的作用.
研究的目的:
- 研究肥胖影响瘤微环境和癌症进展的机制.
- 确定特定的细胞和分子参与肥胖相关癌症发展的参与者.
主要方法:
- 在肥胖的背景下分析与瘤相关的巨细胞 (TAMs).
- 研究G蛋白结合受体65 (GPR65) 在TAM功能中的作用.
- 评估内酸度对TAM和瘤生长的影响.
主要成果:
- 肥胖导致内酸度增加.
- 这种酸度会触发GPR65在瘤相关的巨细胞上升调节.
- 升级的GPR65会损害TAM的效应器功能,从而促进瘤的生长.
结论:
- GPR65是关键的调解者,它将肥胖导致的酸度与瘤微环境中的巨细胞功能受损联系起来.
- 向GPR65或调节内酸性可能代表肥胖相关癌症的新疗法策略.
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