细胞外基质
肿瘤微环境
免疫系统
生物
间质细胞
癌症研究
肿瘤进展
腺癌
免疫疗法
表型
细胞生物学
肺
转录组
动力学(音乐)
核糖核酸
基质
细胞
细胞迁移
免疫学
计算生物学
癌相关成纤维细胞
PD-L1
肺癌
肺腺癌
作者
Bomiao Qing,Xiaolan Li,Xiang He,Junyi Wang,Yi Yang,Manling Jiang,Bingbing Yan,Lei Zhang,Anying Xiong,Qin Ran,Guoping Li
标识
DOI:10.1002/advs.202510847
摘要
Lung adenocarcinoma (LUAD) progression involves dynamic remodeling of the tumor microenvironment (TME). However, the stage-specific dynamics of immune and stromal cell remodeling throughout LUAD progression remain incompletely understood. Here, the study systematically profiles the cellular composition and transcriptional states across multiple LUAD stages, integrating early-stage patient specimens with publicly available datasets encompassing advanced-stage disease. The analysis reveals a marked stage-dependent shift from a proliferative and immune-activated microenvironment in early LUAD to a hypoxia-enriched and immunosuppressive landscape in advanced disease. A distinct hypoxia-adapted epithelial tumor cell subpopulation (C5), exhibiting transcriptional features of metastasis, invasion, and hypoxia, and poor prognosis, is identified. Advanced LUAD featured immunosuppressive LGMN⁺ macrophages and STAT1-driven exhausted CD8⁺ T cells. FKBP11⁺ plasma B cells exhibited exhaustion-linked metabolic changes. POSTN⁺ CAFs emerged as central mediators of extracellular matrix (ECM) remodeling and immune exclusion. Collectively, the findings reveal a model of hypoxia-driven functional convergence, in which distinct TME components co-evolve toward phenotypes that collectively promote immune evasion, matrix remodeling, and tumor progression. These findings may provide insights into stage-specific cellular dynamics and highlight promising therapeutic targets for precision immunotherapy strategies.
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