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通过多组技术阐明NSCLC中的细胞起源和TME动态演变

Ning Ning Chao¹, Li Zhang¹

¹Department of Pulmonary and Critical Care Medicine, Institute of Respiratory Health, State Key Laboratory of Respiratory Health and Multimorbidity, Frontiers Science Center for Disease-related Molecular Network, Sichuan Provincial Engineering Laboratory of Precision Medicine, Precision Medicine Key Laboratory of Sichuan Province, West China Hospital, West China School of Medicine, Sichuan University, Chengdu 610041, Sichuan Province, China.

Biochimica et biophysica acta. Reviews on cancer

|August 21, 2025

概括

先进的多组学揭示了非小细胞肺癌 (NSCLC) 的起源和瘤微环境 (TME) 的动态. 针对血统可塑性和TME重编程提供了针对治疗耐药性的新策略.

科学领域:

癌症学
基因组学
免疫学

背景情况:

非小细胞肺癌 (NSCLC) 仍然是癌症死亡的主要原因.
瘤异质性和微环境重塑会导致免疫疗法和向治疗等现有疗法的耐药性.
了解肺腺癌 (LUAD) 细胞起源和瘤微环境 (TME) 演变对于新的治疗策略至关重要.

研究的目的:

审查多组学方法如何阐明NSCLC的起源和TME动态.
确定推动LUAD进展和治疗耐药性的关键细胞参与者和途径.
探索克服NSCLC治疗耐药性的新兴策略.

主要方法:

单细胞和空间转录组学 (多组学) 分析细胞异质性和空间组织.
瘤微环境 (TME) 组件的分析,包括免疫细胞和癌症相关纤维细胞 (CAF).
针对血统可塑性,TME重编程和微生物组调节的新兴治疗策略的审查.

主要成果:

多组学将膜类型2 (AT2) 细胞确定为LUAD起源,SOX2/WNT/YAP途径介导血统可塑性.
通过免疫编辑演变为TME,CAF/瘤相关的巨细胞 (TAM) 交叉声会促进免疫抑制.
关键的治疗点包括特定的免疫子集 (CXCL13+CD8+T细胞,M1/ M2巨细胞) 和抗原呈现CAF (apCAF).

结论:

提供了对NSCLC演变和TME复杂性的关键见解.
针对谱系可塑性,TME重编程和微生物组调节可以克服对免疫检查点阻塞 (ICB) 和氨酸激酶抑制剂 (TKI) 的抵抗.
以人工智能驱动的TME建模对于解决空间时间异质性和指导NSCLC的精确干预至关重要.

关键词:

免疫编辑血统的可塑性多种类型非小细胞肺癌治疗耐药性瘤微环境

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