ArticleScience translational medicine2020
A YAP/FOXM1 axis mediates EMT-associated EGFR inhibitor resistance and increased expression of spindle assembly checkpoint components.
Article in Science translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers.
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Who cites it
113 citing papers in PubMed.
- YAP/TEAD inhibitor VT3989 in solid tumors: a phase 1/2 trial.Nature medicine · 2025Trial
- Poziotinib for EGFR exon 20-mutant NSCLC: Clinical efficacy, resistance mechanisms, and impact of insertion location on drug sensitivity.Cancer cell · 2022Trial
- DYT8 drives lung adenocarcinoma through EGFR-mediated PSMC6 recruitment and uncharacterized phosphorylation at Ser 306 and 525 of c-Src.Acta pharmacologica Sinica · 2026Article
- MAP2-mediated integrin dysregulation reprograms cancer cell plasticity in hepatocellular carcinoma.Nature communications · 2026Article
- Development of gemcitabine-modified multimodal miR-129 mimic as a novel therapeutic in non-small cell lung cancer.Molecular therapy. Nucleic acids · 2026Article
- Opportunities and challenges in the development of evolving EGFR inhibitors to overcome EGFR TKIs resistance.Acta pharmacologica Sinica · 2026Review
- Covalent pan-TEAD inhibitors block YAP activity and demonstrate brain penetrance in a Hippo-dependent cancer model.Nature communications · 2026Article
- GPNMB-ECD drives acquired resistance to osimertinib in NSCLC via inducing tumor cell cytoskeletal reorganization.Cellular & molecular biology letters · 2026Article
- FOXM1-Specific TCR-Engineered T Cells Target Non-Small Cell Lung Cancer.Cancer immunology research · 2026Article
- Loss of Payload Sensitivity and Other Mechanisms of Resistance to T-DXd in HER2-Mutant NSCLC: Implications for Subsequent Responsiveness to HER2 TKIs.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2026Article
- ELMO2 is a therapeutic vulnerability in mesenchymal-like and drug-resistant non-small cell lung cancer.Nature communications · 2026Article
- Tolerance and Resistance to Targeted Therapy in NSCLC: Emerging Concepts and Strategies.JTO clinical and research reports · 2026Review
- Pleomorphic Carcinoma With EGFR and Concomitant Mutations Transformed From Lung Adenocarcinoma: A Case Report.Cancer reports (Hoboken, N.J.) · 2026Article
- Epithelial-to-mesenchymal transition as a central driver of tumor cell plasticity.Nature cancer · 2026Review
- From Motor Proteins to Oncogenic Factors: The Evolving Role of Kinesin Superfamily Proteins in Breast Cancer Development.Molecular biotechnology · 2026Review
- Osimertinib activates a TGF-β2-dependent secretory program that drives lung adenocarcinoma progression.The Journal of clinical investigation · 2026Article
- Targeting PLK1 potentiates the antitumor efficacy of EGFR-TKIs through inhibiting the JAK1/STAT3 pathway.Cell death & disease · 2026Article
- Drug-tolerant persister cells in cancer: a scoping review of definitions, models, and molecular mechanisms.Frontiers in oncology · 2026Review
- Identification, functional insights and therapeutic targeting of EMT tumour states.Nature reviews. Cancer · 2026Review
- Lung adenocarcinoma surfaceome remodeling with EGFR inhibitors uncovers placental alkaline phosphatase as a target for combination therapy.Cell reports. Medicine · 2025Article
53 more citing papers are in PubMed but not listed here.
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Authors and funding
24 authors.
Funding
Abstract
Acquired resistance to tyrosine kinase inhibitors (TKIs) of epidermal growth factor receptor (EGFR) remains a clinical challenge. Especially challenging are cases in which resistance emerges through EGFR-independent mechanisms, such as through pathways that promote epithelial-to-mesenchymal transition (EMT). Through an integrated transcriptomic, proteomic, and drug screening approach, we identified activation of the yes-associated protein (YAP) and forkhead box protein M1 (FOXM1) axis as a driver of EMT-associated EGFR TKI resistance. EGFR inhibitor resistance was associated with broad multidrug resistance that extended across multiple chemotherapeutic and targeted agents, consistent with the difficulty of effectively treating resistant disease. EGFR TKI-resistant cells displayed increased abundance of spindle assembly checkpoint (SAC) proteins, including polo-like kinase 1 (PLK1), Aurora kinases, survivin, and kinesin spindle protein (KSP). Moreover, EGFR TKI-resistant cells exhibited vulnerability to SAC inhibitors. Increased activation of the YAP/FOXM1 axis mediated an increase in the abundance of SAC components in resistant cells. The clinical relevance of these finding was indicated by evaluation of specimens from patients with EGFR mutant lung cancer, which showed that high
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