来自瘤的外体非编码RNA调节M2巨细胞极化方面的进展:分子机制和信号通路
Yifan Bian1, Jilei Li2, Jiarui Cao1
1Henan University of Chinese Medicine, Zhengzhou, Henan, China.
Cancer medicine
|December 8, 2025
概括
瘤衍生外体 (TEXs) 提供非编码RNA (ncRNAs) 来重新编程巨细胞进入M2免疫抑制状态. 这推动了癌症的进展和治疗耐药性,为免疫疗法提供了新的点.
科学领域:
- 在瘤学瘤学.
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
背景情况:
- 瘤微环境 (TME) 通过免疫抑制促进癌症的进展和治疗耐药性.
- M2巨细胞是免疫抑制TME的关键参与者.
- 瘤衍生异构体 (TEXs) 提供非编码RNA (ncRNAs),驱动M2巨细胞的两极分化.
研究的目的:
- 审查TEX驱动的M2极化分子机制.
- 探索TEX-ncRNA网络与癌症免疫疗法之间的相互作用.
主要方法:
- 系统性文献综述 (2019-2024) 来自PubMed和科学网络.
- 对TEX-ncRNA介导的M2极化所涉及的分子机制和信号通路的分析.
主要成果:
- TEXs向巨细胞传递特定的ncRNA,通过PTEN/PI3Kγ,Wnt/β-catenin和STAT3.3等途径诱导M2极化.
- 由TEXs进行的M2两极化增强了免疫抑制,瘤转移,化学抵抗和免疫逃避.
- 审查了142个引用,其中有60个详细的例子说明了这一机制.
结论:
- 了解TEX-ncRNA网络对于开发新的TME向免疫疗法至关重要.
- 准TEX驱动的M2极化可能会改善耐火性癌症的结果.
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