肥胖期间癌症进展的微环境决定因素:新出现的证据和新的视角
Rossella Salemi1, Valentina Sergi2, Maria Sofia Basile1
1Department of Medicine and Surgery, "Kore" University of Enna, 94100, Enna, Italy.
Journal of translational medicine
|September 24, 2025
概括
肥胖通过改变瘤微环境来加速癌症的进展. 关键的代谢和炎症途径,包括胰岛素/IGF和RAGE信号传递,促进肥胖个体的瘤生长.
科学领域:
- 在瘤学瘤学.
- 代谢综合征是代谢综合征的一种.
- 癌症生物学 癌症生物学
背景情况:
- 肥胖是一种全球流行病,与癌症发病率和死亡率的增加有关.
- 与肥胖相关的代谢失调影响癌细胞生长和瘤微环境 (TME).
- 在癌症的进展中,TME起着至关重要的作用,特别是在肥胖的背景下.
研究的目的:
- 提供有关在肥胖期间TME重编程的关键参与者的概述.
- 突出代谢,分子和细胞因素,促进肥胖患者的癌症进展.
- 强调特定信号通路在肥胖驱动的瘤进化中的作用.
主要方法:
- 文献综述和综合目前关于肥胖,癌症和瘤微环境的研究.
- 分析代谢,分子和细胞机制,将肥胖与癌症进展联系起来.
- 专注于特定的途径:胰岛素/IGF信号传递,VEGF/VEGFR轴和RAGE信号传递.
主要成果:
- 肥胖会重编程TME,促进瘤的生长和进展.
- 肥胖患者的代谢失衡增加了癌细胞的增殖和TME交叉声.
- 激素 (胰岛素/IGF),生长因子 (VEGF/VEGFR) 和炎症 (RAGE) 途径是关键的调解者.
结论:
- 特定的途径显著促进肥胖驱动的瘤微环境进化.
- 了解这些参与者对于开发有针对性的疗法至关重要.
- 需要进一步的研究来应对当前的挑战,并探索与肥胖相关的癌症进展的创新工具.
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