ArticleCommunications biology2021
EGFR Regulates the Hippo pathway by promoting the tyrosine phosphorylation of MOB1.
Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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The trial behind it
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Who cites it
49 citing papers in PubMed, 60 citations in OpenAlex.
- Review
- Positive TAZ-TDG feedback loop drives proneural-to-mesenchymal transition to promote glioblastoma progression.Journal of translational medicine · 2026Article
- ABTB1 modulates EGFR signaling and confers icotinib sensitivity in lung adenocarcinoma.Respiratory research · 2026Article
- Resveratrol as a Novel YAP Inhibitor Targeting Glioblastoma Progression and Sensitizing to Chemotherapy.Cancer science · 2026Article
- Aberrant Hippo-YAP/TEAD Signaling Drives Malignant Transcriptional Reprogramming in External Auditory Canal Squamous Cell Carcinoma.Cancer research communications · 2026Article
- Nuclear Mechanotransduction at the Crossroads: How Membrane Receptors Remodel the Perinuclear Cytoskeleton to Drive Cancer and Disease.International journal of biological sciences · 2026Review
- KSR1 is a scaffold for the Hippo signaling pathway.Communications biology · 2025Article
- YAP as a therapeutic target in esophageal squamous cell carcinoma: insights and strategies.Annals of medicine · 2025Review
- TWF2 Drives Tumor Progression and Sunitinib Resistance in Renal Cell Carcinoma through Hippo Signaling Suppression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Amlodipine exerts inhibitory effects against glioma stem cells through degrading EGFR and down-regulating its downstream pro-survival pathways.Cell death discovery · 2025Article
- The role of phosphatidylinositol (18:1_18:1) in benign prostatic hyperplasia: an integrated study of Mendelian randomization and network pharmacology.World journal of urology · 2025Article
- Histone deacetylase 6: A new player in oxidative stress‑associated disorders and cancers (Review).International journal of molecular medicine · 2025Review
- The components and regulation of the Hippo pathway and its relationships with the progression and treatment of Non-small cell lung cancer (NSCLC).Cancer cell international · 2025Review
- A degradable form of polyoma small T antigen reveals the high specificity of TAZ in regulating gene expression.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Spatially resolved subcellular protein-protein interactomics in drug-perturbed lung-cancer cultures and tissues.Nature biomedical engineering · 2025Article
- Synergistic Enhancement of Osimertinib Efficacy in Non-small Cell Lung Cancer Cells Through Epigallocatechin-3-Gallate: Mechanistic Insights Into YAP/TEAD/CTGF Axis Inhibition.Advanced pharmaceutical bulletin · 2025Article
- An Agrin-YAP/TAZ Rigidity Sensing Module Drives EGFR-Addicted Lung Tumorigenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Targeting YAP/TAZ-TEAD signaling as a therapeutic approach in head and neck squamous cell carcinoma.Cancer letters · 2025Article
- Single-Cell Sequencing Reveals the Role of Radiation-Induced Stemness-Responsive Cancer Cells in the Development of Radioresistance.International journal of molecular sciences · 2025Article
- YAP/TAZ-associated cell signaling - at the crossroads of cancer and neurodevelopmental disorders.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
The Hippo pathway is frequently dysregulated in cancer, leading to the unrestrained activity of its downstream targets, YAP/TAZ, and aberrant tumor growth. However, the precise mechanisms leading to YAP/TAZ activation in most cancers is still poorly understood. Analysis of large tissue collections revealed YAP activation in most head and neck squamous cell carcinoma (HNSCC), but only 29.8% of HNSCC cases present genetic alterations in the FAT1 tumor suppressor gene that may underlie persistent YAP signaling. EGFR is overexpressed in HNSCC and many other cancers, but whether EGFR controls YAP activation is still poorly understood. Here, we discover that EGFR activates YAP/TAZ in HNSCC cells, but independently of its typical signaling targets, including PI3K. Mechanistically, we find that EGFR promotes the phosphorylation of MOB1, a core Hippo pathway component, and the inactivation of LATS1/2 independently of MST1/2. Transcriptomic analysis reveals that erlotinib, a clinical EGFR inhibitor, inactivates YAP/TAZ. Remarkably, loss of LATS1/2, resulting in aberrant YAP/TAZ activity, confers erlotinib resistance on HNSCC and lung cancer cells. Our findings suggest that EGFR-YAP/TAZ signaling plays a growth-promoting role in cancers harboring EGFR alterations, and that inhibition of YAP/TAZ in combination with EGFR might be beneficial to prevent treatment resistance and cancer recurrence.
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Registered trials
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.