ArticleClinical and translational medicine2025
Transitional CXCL14
Article in Clinical and translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- FOXP2+ Chief Cells and CXCL14+ Fibroblasts Drive Fibrotic Remodeling in Carotid Body Tumors.International journal of molecular sciences · 2026Article
- Cytokines and cancer-associated fibroblasts.Journal of hematology & oncology · 2026Review
- Sphingosine-1-Phosphate Receptor 3 Confers Tumor Metastasis in Lung Cancer Resistant to Third-Generation EGFR Inhibitor.MedComm · 2026Article
- IL4I1⁺ Macrophages and TDO2⁺ Myofibroblasts Drive AhR-Mediated Immunosuppression and Ferroptosis Resistance in Solid Predominant Lung Adenocarcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Reciprocal regulation of hMENA and TGF-β signaling in cancer-associated fibroblasts promotes EMT, immunosuppression, poor prognosis, and ICT resistance in NSCLC.Journal for immunotherapy of cancer · 2026Article
- Roles of Cellular Neighborhoods in Lung Cancer.Journal of Cancer · 2026Review
- Fibroblast transformation in the tumor microenvironment of lung adenocarcinoma: heterogeneity, regulation, and therapeutic targeting.Frontiers in immunology · 2026Review
- Cancer-associated fibroblasts in the tumor microenvironment: heterogeneity, crosstalk mechanisms, and therapeutic implications.Molecular cancer · 2025Review
- Cancer-Associated Fibroblasts: Origin, Classification, Tumorigenicity, and Targeting for Cancer Therapy.MedComm · 2025Review
- NUF2 promotes the malignant development of lung adenocarcinoma through the mTORC1 signaling pathway via binding to BUB1B.Journal of thoracic disease · 2025Article
- Review
- Spatial transcriptomics and multi-omics reveal relapse and resistance mechanisms of EndMT-derived CAFs mediated by TNC and FLNC in glioblastoma.Journal of translational medicine · 2025Article
- Transitional CXCL14Clinical and translational medicine · 2025Article
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Authors and funding
17 authors.
Funding
Abstract
backgroundThe heterogeneity of cancer-associated fibroblasts (CAFs) has become a crucial focus in understanding cancer biology and treatment response, revealing distinct subpopulations with specific roles in tumor pathobiology. CAFs have also been shown to promote resistance in lung cancer cells to epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs). However, the specific CAF subsets responsible for driving tumor advancement and resistance to EGFR-TKIs in lung adenocarcinoma (LUAD) remain poorly understood.
methodsWe integrate multiple scRNA-seq datasets to identify cell subclusters most relevant to tumor stage, patient survival, and EGFR-TKIs response. Additionally, in vitro and in vivo experiments, clinical tissue sample immunohistochemistry and patient plasma ELISA experiments are performed to validate key findings in independent LUAD cohorts.
resultsBy analyzing multiple scRNA-seq and spatial transcriptomic datasets, we identified a unique subset of CXCL14+ myofibroblastic CAFs (myCAFs), emerging during the early differentiation phase of pan-cancer invasiveness-associated THBS2⁺ POSTN⁺ COL11A1⁺ myCAFs. Notably, plasma levels of CXCL14 in LUAD patients correlate significantly with tumor stage. Mechanistically, this subset enhances tumor aggressiveness through epithelial-to-mesenchymal transition and angiogenesis. Among standard treatment regimens, transitional CXCL14+ myCAFs specifically confer resistance to EGFR-TKIs, while showing no significant impact on chemotherapy or immunotherapy outcomes. Through a pharmacological screen of FDA-approved drugs, we identified Filgotinib as an effective agent to counteract the EGFR-TKIs resistance conferred by this CAF subset.
conclusionsIn summary, our study highlights the role of the differentiated stage from transitional CXCL14+ myCAFs to invasiveness-associated myCAFs in driving tumor progression and therapy resistance in LUAD, positioning Filgotinib as a promising targeted therapy for this process. These insights may enhance patient stratification and inform precision treatment strategies in LUAD. KEY POINTS: Single-cell analysis identifies transitional CXCL14
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.