ArticleFrontiers in immunology2026
NR2F2 in cancer-associated fibroblasts drives immune microenvironment remodeling and promotes lung adenocarcinoma progression.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: The high heterogeneity of lung adenocarcinoma (LUAD) is largely due to its complex tumor immune microenvironment (TIME). Cancer-associated fibroblasts (CAFs) are a core matrix component of TIME. However, their functional heterogeneity and the specific molecular mechanisms driving tumor progression have not been fully elucidated. In addition, the role of nuclear receptor NR2F2 in tumor development is still controversial. Method: This study integrated scRNA-seq data from the GEO database with RNA-seq data from TCGA and GEO and then performed multiple levels of validation through Result: We noticed the CAF - 2 subgroup, characterized by the highest level of TGF - β signaling activation, sends various signals to different cell types. We constructed and verified a consistent prognostic signature made of 16 genes using the LASSO-Cox method. This model can effectively assess the risk of LUAD patients. The prognosis in high-risk group is worse. And we also do some analysis to find out that risk score is highly associated with immunosuppressive TME and high expressions of PD - L1. We have found in our further study that the expression of NR2F2 in CAF is associated with the promoting of matrix remodeling and metabolic reprogramming. From the coculture system and Conclusion: Using single-cell RNA sequencing data, we identified a CAF subgroup with the most active TGF-β signaling. Based on the marker genes of the subgroup, we constructed and validated an effective prognostic model, then we further screened and confirmed NR2F2 as a major pro-tumorigenic regulator from this feature gene set through single cell and transcriptome data as well as
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