ArticleOncogene2025
Senescent lung fibroblasts in idiopathic pulmonary fibrosis facilitate non-small cell lung cancer progression by secreting exosomal MMP1.
Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed.
- A serum proteomics-based predictive model for steroid-resistant immune checkpoint inhibitor associated myocarditis.Clinical and translational medicine · 2026Article
- Extracellular vesicles in senescence-associated chronic lung diseases.Chinese medical journal · 2026Review
- Convergent Microenvironment Linking Idiopathic Pulmonary Fibrosis and Lung Cancer.Expert reviews in molecular medicine · 2026Review
- Cellular Senescence: Emerging Therapeutic Target for Idiopathic Pulmonary Fibrosis Pathogenic Mechanisms and Therapeutic Strategies.Biomolecules & therapeutics · 2026Review
- TMEM33 regulates the proliferation and migration of lung adenocarcinoma by promoting the PI3K/AKT/mTOR signaling pathway.Cancer cell international · 2026Article
- Hallmarks of the ageing lung: 10 years later.The European respiratory journal · 2026Review
- Micro-Nanoplastic Exposure and Lung Cancer Biomarkers: The Role of Extracellular Vesicle-Mediated Intercellular Communication.International journal of molecular sciences · 2026Review
- Lactate metabolism and lactylation in cancer: from pathogenesis to therapeutic advances.Signal transduction and targeted therapy · 2026Review
- Photocrosslinkable lung dECM hydrogels promote stiffness-dependent lung cancer growth and chemoresistance.Materials today. Bio · 2026Article
- Review
- Greater susceptibility of patients with idiopathic pulmonary fibrosis to basal cell carcinoma: a combined genomics and Mendelian randomization analysis.Translational cancer research · 2026Article
- The Fibrotic-Cancer Continuum in IPF: Shared Mechanisms, Clinical Implications and Therapeutic Challenges.Life (Basel, Switzerland) · 2026Review
- Research progress of MicroRNA in lung cancer.Discover oncology · 2026Review
- 20-hydroxyecdysone promotes brain development via upregulating MMP2 expression during metamorphosis in Helicoverpa armigera.PLoS genetics · 2026Article
- Breaking barriers in pulmonary health of patients with metabolic diseases: senolytics and beyond.Frontiers in aging · 2026Review
- Network toxicology reveals key genes of amiodarone induced pulmonary fibrosis: based on machine learning and SHAP analysis.Frontiers in pharmacology · 2026Article
- Roles of exosomes in microenvironment-related premature ovarian insufficiency: mechanisms and therapeutic intervention.Reproductive biology and endocrinology : RB&E · 2025Review
- Insight into the pathogenesis of interstitial lung diseases and near-to-native lung fibrosis models.European journal of medical research · 2025Review
- Aging and lung diseases: Unraveling mechanisms and therapeutic targets.Chinese medical journal pulmonary and critical care medicine · 2025Review
- From Fibrosis to Malignancy: Mechanistic Intersections Driving Lung Cancer Progression.Cancers · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Lung cancer is a fatal complication of idiopathic pulmonary fibrosis (IPF) with a poor prognosis. Current treatments are insufficient in improving the prognosis of lung cancer patients with comorbid idiopathic pulmonary fibrosis (IPF-LC). Senescent fibroblasts, as stromal cells in the tumor microenvironment, influence tumor progression via exosomes. With evidence that fibroblast senescence is an important mechanism of IPF, we investigated the impact of senescent IPF lung fibroblast (diseased human lung fibroblasts, DHLF)-derived exosomes on non-small cell lung cancer (NSCLC). We found DHLF expressed significant senescence markers, and promoted NSCLC proliferation, invasion, and epithelial-mesenchymal transition. Specifically, senescent DHLF showed strong secretion of exosomes, and these exosomes enhanced the proliferation and colony-forming ability of cancer cells. Proteomic analysis showed DHLF-derived exosomes exhibited upregulated senescence-associated secretory phenotype (SASP) factors, notably MMP1, which activates the surface receptor PAR1. Knocking down MMP1 or using PAR1 inhibitors reduced the tumor-promoting effects of DHLF-derived exosomes in vivo and in vitro. Mechanistically, MMP1 acted by activating the PI3K-AKT-mTOR pathway. In conclusion, our results suggest that exosomal MMP1 derived from senescent IPF fibroblasts promotes NSCLC proliferation and colony formation by targeting PAR1 and activating the PI3K-AKT-mTOR pathway. These findings provide a novel therapeutic approach for patients with IPF-LC.
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