ArticleOncology research2025
Single-Cell Transcriptomic Profiling Reveals KRAS/TP53-Driven Neutrophil Reprogramming in Luad: A Multi-Gene Prognostic Model and Therapeutic Targeting of RHOV.
Article in Oncology research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Differential transcriptomic modulation by histone deacetylase inhibitor SAHA in LUAD and LUSC.Clinical epigenetics · 2026Article
- Identify novel molecular subtypes of lung adenocarcinoma to predict treatment response and prognosis.Scientific reports · 2025Article
- Neutrophils in non-small cell lung cancer and immunotherapy with PD-1/PD-L1 inhibitors.Journal of translational medicine · 2025Review
- Immune-Like Malignant Epithelial Programs Shape Tumor-Immune Interactions and Inform Prognostic Stratification in Lung Adenocarcinoma.BioFactors (Oxford, England)Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: The tumorigenic progression of Lung adenocarcinoma (LUAD), the predominant NSCLC subtype, is predominantly driven by co-occurring mutations in KRAS proto-oncogene (KRAS)/Tumor protein p53 (TP53). However, their impact on tumor microenvironment (TME) heterogeneity, particularly neutrophil dynamics, remains poorly understood. This present study aims to elucidate how KRAS/TP53 mutations reprogram the TME and develop a neutrophil-centric prognostic signature for LUAD. Methods: Leveraging single-cell RNA sequencing data and transcriptome data, neutrophil subpopulations were identified using Seurat and CellChat R packages, with trajectory analysis via Monocle2 R package. High-dimensional weighted gene co-expression network analysis (hdWGCNA), univariate Cox regression, and least absolute shrinkage and selection operator (LASSO) regression analyses were employed to generate a prognostic signature. Functional validation included Ras homolog family member V (RHOV) knockdown in A549/H1299 cells using siRNA, were assessed by cell counting kit 8 (CCK8) assay, wound healing assay, and transwell assay. Results: KRAS/TP53-mutated LUAD exhibited increased neutrophil infiltration, particularly IS MUT subtypes with enhanced OSM/CALCR/IL-1 signaling. A five-gene prognostic signature (MS4A1, ANLN, FAM83A, RHOV, KRT6A) stratified patients into high- and low-risk groups with divergent overall survival in the TCGA-LUAD cohort ( Conclusion: KRAS/TP53 mutations may drive neutrophil heterogeneity in the TME of LUAD, addressing prognostic and therapeutic value. The five-gene signature and RHOV targeting offer translational relevance for risk stratification and therapy. These findings bridge genomic alterations with TME remodeling, advancing precision oncology in LUAD.
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