ArticleNature communications2025
A human model to deconvolve genotype-phenotype causations in lung squamous cell carcinoma.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Sex determining region Y box protein 2 (SOX2) expression, alteration, regulation and its diagnostics, prognostics and therapeutics in lung cancer.Discover oncology · 2026Article
- The role of the tumor microenvironment in drug resistance acquisition in lung squamous cell carcinoma.Journal of experimental & clinical cancer research : CR · 2026Review
- The identification of RNA splicing aberrations and their potential regulatory network in Chinese non-small cell lung cancer.Respiratory research · 2026Article
- Transcriptional activation of PPP1R14C by KLF7 unleashes CDK1 activity to promote lung squamous cell carcinoma.Scientific reports · 2026Article
- RPSLearner: A Novel Approach Based on Random Projection and Deep Stacking Learning for Categorizing Non-Small Cell Lung Cancer.Advanced intelligent systems (Weinheim an der Bergstrasse, Germany) · 2026Article
- Gene amplification in the premalignant stages of non-small cell lung cancer development.Frontiers in oncology · 2026Review
- Cholesterol Regulates Airway Epithelial Cell Differentiation by Inhibiting p53 Nuclear Translocation.International journal of molecular sciences · 2025Article
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Authors and funding
7 authors.
Funding
Abstract
Tractable, patient-relevant models are needed to investigate cancer progression and heterogeneity. Here, we report an alternative in vitro model of lung squamous cell carcinoma (LUSC) using primary human bronchial epithelial cells (hBECs) from three healthy donors. The co-operation of ubiquitous alterations (TP53 and CDKN2A loss) and components of commonly deregulated pathways including squamous differentiation (SOX2), PI3K signalling (PTEN) and the oxidative stress response (KEAP1) is investigated by generating hBECs harbouring cumulative alterations. Our analyses confirms that SOX2-overexpression initiates early preinvasive LUSC stages, and co-operation with the oxidative stress response and PI3K pathways to drive more aggressive phenotypes, with expansion of cells expressing LUSC biomarkers and invasive properties. This cooperation is consistent with the classical LUSC subtype. Importantly, we connect pathway dysregulation with gene expression changes associated with cell-intrinsic processes and immunomodulation. Our approach constitutes a powerful system to model LUSC and unravel genotype-phenotype causations of clinical relevance.
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