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Life sciences · Journal article
Journal of Experimental & Clinical Cancer Research · October 6, 2026
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Abstract Background The tumor microenvironment (TME) in non-small cell lung cancer (NSCLC) exhibits heterogeneity across distinct oncogenic driver mutations, but whether specific stromal states are shaped by these mutations and how they influence tumor progression and therapy response remains inadequately understood. Methods We integrated single-cell RNA sequencing (scRNA-seq) and single-cell spatial transcriptomic analyses of NSCLC samples to characterize mutation-associated TME reprogramming. In vitro and in vivo molecular assays were performed to elucidate the mechanisms driving tumor proliferation. Results Our analysis identified a fibroblast subpopulation enriched in EGFR -mutant NSCLC, termed Fib_COL16A1, which is transcriptionally maintained by SMAD3, evolutionarily conserved (as Fib_Col16a1 in murine NSCLC models), and functions as an independent prognostic marker for poor survival. Fib_COL16A1 spatially colocalizes with both tumor cells and CD8⁺ T cells. Mechanistically, Fib_COL16A1 drives tumor growth in EGFR -mutant NSCLC by enhancing tumor cell proliferation and promoting CD8⁺ T-cell exhaustion via the COL16A1-integrin β1 signaling axis. Therapeutic targeting of this axis impedes tumor progression as well as enhances sensitivity to both osimertinib and pembrolizumab. Conclusion This study reveals a mutation-specific stromal-tumor-immune regulatory network and establishes the COL16A1-integrin β1 pathway as a rational therapeutic target to enhance the efficacy of osimertinib and pembrolizumab in EGFR -mutant NSCLC.