ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
EGFR-TKIs Induced DPP4 Drives Metabolic Reprogramming of Persister Cells in Lung Cancer.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Post-translational modifications in metabolic reprogramming: implications for metabolic therapy and immunotherapy in cancer.Signal transduction and targeted therapy · 2026Review
- CD26 + CD39 - CD73 + CD4 + T lymphocytes decrease after HIV-1 infection but show an intrinsic association with low viral replication and high CD4 + T-cell count.Chinese medical journal · 2026Article
- Cancer drug response and resistance: molecular mechanisms and combating strategies.Signal transduction and targeted therapy · 2026Review
- Recent advances in engineered nanozymes for precision lung cancer therapy.Materials today. Bio · 2026Review
- Plasticity of Non-Apoptotic Residual Tumor Cells After Neoadjuvant Immunochemotherapy: Epigenetic and Microenvironmental Determinants.Biomolecules · 2026Review
- Reciprocal signaling-metabolic crosstalk between fibroblasts and tumor cells drives cetuximab tolerance in head and neck cancers.Journal of experimental & clinical cancer research : CR · 2026Article
- Therapeutic strategies for MMAE-resistant bladder cancer through DPP4 inhibition.Molecular oncology · 2026Article
- Epigenetic modifications in cancer drug resistance: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Article
- Single-cell and spatial omics in non-small cell lung cancer: dissecting metabolic reprogramming and tumor-immune ecosystems for precision pharmacology.Frontiers in immunology · 2026Review
- Mitochondrial niches of residual disease in EGFR-mutant NSCLC: immune-constrained persistence and therapeutic interception.Frontiers in immunology · 2026Review
- Advances in understanding the mechanisms underlying acquired resistance to third-generation tyrosine kinase inhibitors in non-small cell lung cancer.Frontiers in cell and developmental biology · 2026Review
- Mitochondrial metabolic-transcriptional axis drives adaptive drug tolerance across major lung cancer subtypes.Frontiers in genetics · 2026Review
- Advances in Metabolic Reprogramming and Immune Regulatory Mechanisms in Lung Cancer.Oncology research · 2026Review
- Drug-tolerant persister cells: the deadly survivors in hematological malignancies.Frontiers in pharmacology · 2026Review
- Progression and Metastasis of Lung Cancer: Clinical Features, Molecular Mechanisms, and Clinical Managements.MedComm · 2025Review
- EGFR-TKIs Induced DPP4 Drives Metabolic Reprogramming of Persister Cells in Lung Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- [Applications and Advances of Metabolomics in Lung Cancer Research].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2025Review
- Palmitoylation in cancer: decoding its roles in signal transduction, tumor immunity, and emerging therapeutic opportunities.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Mutations in epidermal growth factor receptor (EGFR) are the key drivers of lung cancer initiation and recurrence. The cancer cells undergo transformation to a reversible drug-tolerant persister (DTP) state prior to the development of resistance against EGFR-tyrosine kinase inhibitors (TKIs). Two DTP lung cancer cells with different proliferative capacities are established and identified dipeptidyl peptidase 4 (DPP4) as a potential therapeutic target. The DTP cells primarily relied on oxidative phosphorylation, which is accompanied by the up-regulation of fatty acid metabolism. Mechanistically, DPP4 facilitates the uptake of fatty acids via carnitine palmitoyl transferase 1a (CPT1A, and enhances fatty acid oxidation. In addition, the DPP4-mitogen-activated protein kinase kinase (MEK)-Nuclear factor erythroid-2-related factor 2 (Nrf2) signaling pathway maintains mitochondrial function by activating the antioxidant pathway. The combination of osimertinib and sitagliptin, a DPP4 inhibitor, not only suppressed tumor progression but also reduced the number of residual tumor cells and minimal residual disease. Notably, this combination therapy significantly lowered recurrence rates and extended the survival of tumor-bearing mice compared to the monotherapies. The study provides new insights into the metabolic adaptations of DTP lung cancer cells in response to EGFR-TKIs, offering novel therapeutic strategies for targeting these persister cells.
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