ArticleFrontiers in cell and developmental biology2026
A single-cell sequencing-based prognostic model reveals HLA-DRA, NPC2, and PRPF38B as immune-regulatory tumor suppressors in non-small cell lung cancer.
Article in Frontiers in cell and developmental biology, 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: Non-small cell lung cancer (NSCLC) is the most common lung cancer subtype and a leading cause of cancer-related mortality due to asymptomatic early stages and poor 5-year survival, and tumor-infiltrating lymphocytes (TILs) play a pivotal but poorly defined role in NSCLC progression and prognosis within the tumor microenvironment (TME). Methods: We analyzed single-cell RNA sequencing data from GEO (GSE148466), NSCLC-related data from TCGA, and gene expression data from GEO (GSE50081). A 9-gene TIL-related risk score model (HLA-DRA, NPC2, PRPF38B, PABPC1, ENO1, ANXA2, LGALS1, S100A10, SRGN) was constructed using LASSO regression, with its prognostic value assessed via Kaplan-Meier and ROC analyses and external validation. Immune infiltration and regulatory factors were analyzed using TISIDB, pathway associations via GSVA and GSEA, and functional roles of key genes (HLA-DRA, NPC2, PRPF38 B) validated using RT-qPCR, Western blotting, and co-culture assays. Results: TILs were abundant in both smoking and non-smoking NSCLC samples. The 9-gene risk model effectively stratified patients by survival, with high-risk patients showing poorer outcomes and enriched tumor-promoting immune features and pathways. High-risk scores were associated with increased M0 macrophages, activated NK cells, and elevated immune checkpoints. Overexpression of HLA-DRA, NPC2, and PRPF38 B inhibited NSCLC cell proliferation, migration, and invasion, while enhancing apoptosis and suppressing M2 macrophage polarization. Conclusion: This study establishes a TIL-based prognostic risk model for NSCLC and identifies HLA-DRA, NPC2, and PRPF38 B as potential immune-regulatory therapeutic targets with tumor-suppressive functions, providing new insights for NSCLC precision immunotherapy.
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