ArticleNature communications2022
Club cells employ regeneration mechanisms during lung tumorigenesis.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- Lineage identity governs oncogene dependence in mouse NSCLC models of KRAS inhibitor resistance.Nature genetics · 2026Article
- Hallmarks of lung cancer driven by inhalable particulate matter: From cell-intrinsic oncogenic traits to microenvironment remodeling.Innovation (Cambridge (Mass.)) · 2026Review
- PRKCI-ECT2 copy number gain promotes developmental reprogramming and metastatic competence in lung adenocarcinoma.Cell reports · 2026Article
- The Gut-Lung Microbiome Axis in Alveolar Stem Cell Regeneration and Lung Repair.Microorganisms · 2026Review
- Single-cell RNA sequencing of hematopoietic and non-hematopoietic cells defines a distinct signature in atopic and NRG1 mouse lung.Scientific reports · 2026Article
- scTACL: a multitask topology-aware contrastive learning approach for single-cell transcriptomics analysis.Bioinformatics (Oxford, England) · 2026Article
- Lineage plasticity: a new dilemma in lung cancer treatment.Molecular biology reports · 2026Review
- EML4-ALK Variant-Specific Genetic Interactions Shape Lung Tumorigenesis.Cancer discovery · 2026Article
- The repressor Capicua is a barrier to lung tumor development driven by Kras/Trp53 mutations.EMBO molecular medicine · 2025Article
- Efficient and multiplexed somatic genome editing with Cas12a mice.Nature biomedical engineering · 2025Article
- ERG-driven prostate cancer initiation is cell-context dependent and requires KMT2A and DOT1L.Nature genetics · 2025Article
- Persistent lineage plasticity driving lung cancer development and progression.Clinical and translational medicine · 2025Review
- CellMemory: hierarchical interpretation of out-of-distribution cells using bottlenecked transformer.Genome biology · 2025Article
- Acquisition of discrete immune suppressive barriers contributes to the initiation and progression of preinvasive to invasive human lung cancer.bioRxiv : the preprint server for biology · 2025Article
- Emerging strategies to investigate the biology of early cancer.Nature reviews. Cancer · 2024Review
- Enhancing peptide and PMO delivery to mouse airway epithelia by chemical conjugation with the amphiphilic peptide S10.Molecular therapy. Nucleic acids · 2024Article
- Tumor initiation and early tumorigenesis: molecular mechanisms and interventional targets.Signal transduction and targeted therapy · 2024Review
- Cellular Origins and Lineage Plasticity in Cancer.Cold Spring Harbor perspectives in medicine · 2024Review
- Evolving insights into the improvement of adoptive T-cell immunotherapy through PD-1/PD-L1 blockade in the clinical spectrum of lung cancer.Molecular cancer · 2024Review
- Physiological and immunological barriers in the lung.Seminars in immunopathology · 2024Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The high plasticity of lung epithelial cells, has for many years, confounded the correct identification of the cell-of-origin of lung adenocarcinoma (LUAD), one of the deadliest malignancies worldwide. Here, we employ lineage-tracing mouse models to investigate the cell of origin of Eml4-Alk LUAD, and show that Club and Alveolar type 2 (AT2) cells give rise to tumours. We focus on Club cell originated tumours and find that Club cells experience an epigenetic switch by which they lose their lineage fidelity and gain an AT2-like phenotype after oncogenic transformation. Single-cell transcriptomic analyses identified two trajectories of Club cell evolution which are similar to the ones used during lung regeneration, suggesting that lung epithelial cells leverage on their plasticity and intrinsic regeneration mechanisms to give rise to a tumour. Together, this study highlights the role of Club cells in LUAD initiation, identifies the mechanism of Club cell lineage infidelity, confirms the presence of these features in human tumours, and unveils key mechanisms conferring LUAD heterogeneity.
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