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Treatment-Induced Tumor Dormancy through YAP-Mediated Transcriptional Reprogramming of the Apoptotic Pathway
Open accessAbstract
Eradicating tumor dormancy that develops following epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) treatment of EGFR-mutant non-small cell lung cancer, is an attractive therapeutic strategy but the mechanisms governing this process are poorly understood. Blockade of ERK1/2 reactivation following EGFR TKI treatment by combined EGFR/MEK inhibition uncovers cells that survive by entering a senescence-like dormant state characterized by high YAP/TEAD activity. YAP/TEAD engage the epithelial-to-mesenchymal transition transcription factor SLUG to directly repress pro-apoptotic BMF, limiting drug-induced apoptosis. Pharmacological co-inhibition of YAP and TEAD, or genetic deletion of YAP1, all deplete dormant cells by enhancing EGFR/MEK inhibition-induced apoptosis. Enhancing the initial efficacy of targeted therapies could ultimately lead to prolonged treatment responses in cancer patients.
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“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 [29]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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 [29]
Experimental — accuracy not yet measuredIn the citing paper
“the authors observed that after treatment with the combination of EGFR and MEK inhibitors, the vast majority of barcodes were unique, suggesting that the ability of cells to enter dormancy following dual inhibition of EGFR and MEK is predominately driven by a stochastic process [56].”
From Emerging Insights into Targeted Therapy-Tolerant Persister Cells in Cancer (2021) · cites this paper as [56]
In the citing paper
“The results revealed a large fraction of shared barcodes within the cells treated with EGFR inhibitor alone, consistent with selection of pre-existing persister clones.”
From Emerging Insights into Targeted Therapy-Tolerant Persister Cells in Cancer (2021) · cites this paper as [56]
In the citing paper
“Meanwhile, other studies suggest that some persister phenotypes arise via plasticity induced by drug treatment [56,64,65].”
From Emerging Insights into Targeted Therapy-Tolerant Persister Cells in Cancer (2021) · cites this paper as [56]
In the citing paper
“Kurppa et al. observed that combined EGFR/MEK inhibition of EGFR-mutant NSCLC model cells selected a population of dormant drug-tolerant cells exhibiting senescence-like features characterized by high YAP/TEAD activity [56].”
From Emerging Insights into Targeted Therapy-Tolerant Persister Cells in Cancer (2021) · cites this paper as [56]
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Metadata
- Authors
- Kurppa, K. J., Liu, Y., To, C., Zhang, T., Fan, M., Vajdi, A., Knelson, E. H., Xie, Y., Lim, K., Cejas, P., Portell, A., Lizotte, P. H., Ficarro, S. B., Li, S., Chen, T., Haikala, H. M., Wang, H., Bahcall, M., Gao, Y., Shalhout, S., Boettcher, S., Shin, B. H., Thai, T., Wilkens, M. K., Tillgren, M. L., Mushajiang, M., Xu, M., Choi, J., Bertram, A. A., Ebert, B. L., Beroukhim, R., Bandopadhayay, P., Awad, M. M., Gokhale, P. C., Kirschmeier, P. T., Marto, J. A., Camargo, F. D., Haq, R., Paweletz, C. P., Wong, K.-K., Barbie, D. A., Long, H. W., Gray, N. S., & Jänne, P. A.
- Affiliations
- Harvard University (US)
- Dana-Farber Cancer Institute (US)
- Brigham and Women's Hospital (US)
- NYU Langone Health (US)
- Tongji University (CN)
- Boston Children's Hospital (US)
- Broad Institute (US)
- ORCID
- Kurppa, Kari J.
- Liu, Yao
- To, Ciric
- Zhang, Tinghu
- Fan, Mengyang
- Vajdi, Amir
- Knelson, Erik H.
- Xie, Yingtian
- Lim, Klothilda
- Cejas, Paloma
- Portell, Andrew
- Lizotte, Patrick H.
- Ficarro, Scott B.
- Li, Shuai
- Chen, Ting
- Haikala, Heidi M.
- Wang, Haiyun
- Bahcall, Magda
- Gao, Yang
- Shalhout, Sophia
- Boettcher, Steffen
- Shin, Bo Hee
- Thai, Tran
- Wilkens, Margaret K.
- Xu, Man
- Choi, Jihyun
- Bertram, Arrien A.
- Ebert, Benjamin L.
- Beroukhim, Rameen
- Bandopadhayay, Pratiti
- Awad, Mark M.
- Gokhale, Prafulla C.
- Marto, Jarrod A.
- Camargo, Fernando D.
- Haq, Rizwan
- Paweletz, Cloud P.
- Wong, Kwok-Kin
- Barbie, David A.
- Long, Henry W.
- Gray, Nathanael S.
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2020-01
- Volume
- 37
- Issue
- 1
- Pages
- 104-122.e12
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC7146079
- OpenAlex
- W3000285141
- Cited by
- 475
- References
- 92
- Citations by year
- 2026: 50 · 2025: 94 · 2024: 82 · 2023: 81 · 2022: 71 · 2021: 65 · 2020: 30
- FWCI
- 30.92
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- UTUPub (University of Turku) (submittedVersion)
- Funders
- National Cancer Institute (NIH 5 P30 CA06516, R01CA135257, R35CA220497)
- Novartis Institutes for BioMedical Research
- Bristol-Myers Squibb
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
- Eli Lilly and Company
- Daiichi Sankyo Company
- Astellas Pharma US
- Dana-Farber/Harvard Cancer Center
- American Cancer Society (CRP-17-111-01-CDD)
- Takeda Oncology
- Massachusetts Institute of Technology
- Instrumentariumin Tiedesäätiö
- Takeda Pharmaceuticals U.S.A.
- National Science Foundation (P300PB_161026/1, P400PM_183862)
- Dana-Farber Cancer Institute
- National Institutes of Health (CA233800, R01 CA222218)
- Jane ja Aatos Erkon Säätiö
- Novartis
- Krebsliga Schweiz (KLS-3625-02 2015)
- Sanofi
- Orionin Tutkimussäätiö
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Melanoma and MAPK Pathways
- Keywords
- tumor dormancy, EGFR tyrosine kinase inhibitors, EGFR-mutant non-small cell lung cancer, MEK inhibition, Slug, BMF, apoptosis, transcriptional reprogramming, drug resistance
- MeSH terms
- YAP-Signaling Proteins, Animals, Cell Survival, Female, Humans, Lung Neoplasms, Male, Mutation, Transcription Factors, Transcription, Genetic, Signal Transduction, Gene Expression Regulation, Neoplastic, Cellular Senescence, Apoptosis, Gene Deletion, Mice, Knockout, Cell Cycle Proteins, Drug Resistance, Neoplasm, Cell Line, Tumor, MAP Kinase Kinase 1, Adaptor Proteins, Signal Transducing, Cell Proliferation, Mice, ErbB Receptors
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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