脂肪衍生性干细胞和与癌症相关的纤维细胞:瘤进展中的相互作用和影响
Rasha S Abo El Alaa1, Wafaa Al-Mannai1, Nour Darwish1
1Biomedical Research Centre, Qatar University, Doha P.O. Box 2713, Qatar.
International journal of molecular sciences
|November 9, 2024
概括
在瘤微环境 (TME) 中,脂质衍生性树皮细胞 (ASC) 可以成为与癌症相关的纤维细胞 (CAF). 这种可塑性推动了癌症的进展,侵入性和耐药性,突出了新的治疗点.
科学领域:
- 在瘤学瘤学.
- 细胞生物学 细胞生物学
- 癌症研究 癌症研究
背景情况:
- 脂肪酸衍生性树皮细胞 (ASC) 和癌症相关纤维细胞 (CAF) 是瘤微环境 (TME) 的关键组成部分.
- 这些细胞显著影响癌症的进展,转移和治疗耐药性.
- ASCs表现出可塑性,能够在瘤衍生的信号下转化为CAF.
研究的目的:
- 审查ASC和CAF在癌症进展中的多方面的作用.
- 探索驱动ASC-CAF转差的机制及其对瘤生物学的影响.
- 确定针对ASC和CAF的潜在治疗策略,以改善癌症治疗结果.
主要方法:
- 关于ASC,CAF及其在TME中的相互作用的文献综述.
- 对参与EMT和CAF激活的关键信号通路 (TGF-β,Wnt/β-catenin,Notch) 的分析.
- 检查ASC和CAF中的表观遗传修饰和代谢重编程.
- 讨论针对这些细胞和分子参与者的治疗策略.
主要成果:
- ASCs转化为CAFs,通过细胞外基质重塑和促炎性细胞因子分泌促进瘤发生.
- ASCs和CAFs促进了上皮细胞向介质酶细胞的过渡 (EMT),增强了癌细胞的侵入性和治疗耐药性.
- 关键的信号通路,表观遗传变化和代谢重编程对于ASC/CAF前瘤功能至关重要.
- 针对这些通路和细胞功能提供了潜在的治疗途径.
结论:
- 了解ASC和CAF在TME中的可塑性和功能,对于开发新型癌症疗法至关重要.
- 破坏ASC-CAF相互作用及其亲瘤源机制可以改善患者的治疗结果.
- 向性抑制剂和免疫疗法是抵消ASC和CAFs促癌效应的有希望的策略.
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