A YAP/FOXM1 axis mediates EMT-associated EGFR inhibitor resistance and increased expression of spindle assembly checkpoint components
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YAP and FOXM1 are mediators of EGFR inhibitor resistance, and spindle proteins are therapeutic targets for this multidrug-resistant phenotype.
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YAP/TAZ plays a crucial role in intrinsic and acquired resistance to inhibitors targeting the RTK/MAPK pathway.
“Particularly, YAP/TAZ plays a crucial role in the intrinsic and acquired resistance to inhibitors targeting RTK/MAPK pathway (24, 28–32).”
From YAP/TAZ mediates resistance to KRAS inhibitors through inhibiting proapoptosis and activating the SLC7A5/mTOR axis (2024) · cites this paper as [28]
The Discussion (page not supplied) reports increased YAP activity in cells with acquired, EGFR-independent resistance to EGFR inhibitors, and the Results describe increased YAP activity in early drug-tolerant persister cells. This supports a role for YAP in EGFR inhibitor resistance, but the paper does not establish a role for TAZ or intrinsic resistance, or extend its finding to RTK/MAPK-targeting inhibitors generally. (LLM, conf=0.87)
Experimental — accuracy not yet measuredDysregulation of the Hippo-YAP/TAZ pathway serves as a central resistance mechanism in multiple therapies, particularly intrinsic and acquired resistance to RTK, RAF, or MEK inhibitors.
“accumulating evidence suggests that the dysregulation of the Hippo-YAP/TAZ pathway serves as a central resistance mechanism in multiple therapies, particularly in the intrinsic and acquired resistance to RTK, RAF, or MEK inhibitors (24, 28, 29).”
From YAP/TAZ mediates resistance to KRAS inhibitors through inhibiting proapoptosis and activating the SLC7A5/mTOR axis (2024) · cites this paper as [28]
The Discussion (page unavailable) identifies YAP as a contributor to acquired EGFR TKI resistance, and the Results report that resistant cells also resisted a range of other kinase inhibitors. The paper does not establish YAP/TAZ dysregulation as a central mechanism of intrinsic and acquired resistance across RTK, RAF, and MEK inhibitors; its mechanistic findings focus on acquired EGFR inhibitor resistance. (LLM, conf=0.87)
Experimental — accuracy not yet measuredActivation of a YAP/FOXM1 axis in EMT EGFR TKI-resistant models is associated with dysregulation of spindle assembly checkpoint (SAC) proteins, including polo-like kinase 1, aurora kinases, and kinesin spindle protein, and renders cells vulnerable to SAC inhibitors.
“Nilsson et al. identified activation of a YAP/FOXM1 axis in EMT EGFR TKI-resistant models [91]. This was associated with dysregulation of spindle assembly checkpoint (SAC) proteins, including polo-like kinase 1, aurora kinases, and kinesin spindle protein, and rendered cells vulnerable to SAC inhibitors.”
From Emerging Insights into Targeted Therapy-Tolerant Persister Cells in Cancer (2021) · cites this paper as [91]
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- Authors
- Nilsson, M. B., Sun, H., Robichaux, J., Pfeifer, M., McDermott, U., Travers, J., Diao, L., Xi, Y., Tong, P., Shen, L., Hofstad, M., Kawakami, M., Le, X., Liu, X., Fan, Y., Poteete, A., Hu, L., Negrao, M. V., Tran, H., Dmitrovsky, E., Peng, D., Gibbons, D. L., Wang, J., & Heymach, J. V.
- Affiliations
- The University of Texas MD Anderson Cancer Center (US)
- AstraZeneca (United Kingdom) (GB)
- Departments of Thoracic/Head and Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
- Corresponding author
- Heymach, John V.
- ORCID
- Nilsson, Monique B.
- Sun, Huiying
- Robichaux, Jacqulyne
- Pfeifer, Matthias
- McDermott, Ultan
- Travers, Jon
- Diao, Lixia
- Xi, Yuanxin
- Tong, Pan
- Shen, Li
- Hofstad, Mia
- Kawakami, Masanori
- Le, Xiuning
- Liu, Xi
- Fan, Youhong
- Poteete, Alissa
- Hu, Limei
- Negrao, Marcelo V.
- Tran, Hai
- Dmitrovsky, Ethan
- Peng, David
- Gibbons, Don L.
- Wang, Jing
- Heymach, John V.
- Venue
- Science Translational Medicine
- Published
- 2020-09-02
- Volume
- 12
- Issue
- 559
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- PMC
- PMC8269000
- OpenAlex
- W3082143929
- Cited by
- 177
- References
- 74
- Citations by year
- 2026: 15 · 2025: 34 · 2024: 29 · 2023: 40 · 2022: 31 · 2021: 26 · 2020: 2
- FWCI
- 14.23
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (Lung SPORE grant P50 CA070907, NIH CCSG (CA016672), CA016672, 1R01 CA190628)
- National Cancer Institute (HHSN261200800001E)
- LUNGevity Foundation
- University of Texas MD Anderson Cancer Center (Lung Cancer Moon Shot Program)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
- Health Sciences › Medicine › Oncology › HER2/EGFR in Cancer Research
- Keywords
- epithelial-mesenchymal transition, EGFR tyrosine kinase inhibitor resistance, spindle assembly checkpoint, multidrug resistance, therapeutic vulnerabilities, non-small cell lung cancer, clinical outcomes
- MeSH terms
- Forkhead Box Protein M1, Antineoplastic Agents, Carcinoma, Non-Small-Cell Lung, Humans, Lung Neoplasms, Drug Resistance, Neoplasm, Proteomics, Cell Line, Tumor, Protein Kinase Inhibitors, Epithelial-Mesenchymal Transition, M Phase Cell Cycle Checkpoints, ErbB Receptors
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