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β-Catenin-Driven Cancers Require a YAP1 Transcriptional Complex for Survival and Tumorigenesis
Open accessAbstract
Wnt/β-catenin signaling plays a key role in the pathogenesis of colon and other cancers; emerging evidence indicates that oncogenic β-catenin regulates several biological processes essential for cancer initiation and progression. To decipher the role of β-catenin in transformation, we classified β-catenin activity in 85 cancer cell lines in which we performed genome-scale loss-of-function screens and found that β-catenin active cancers are dependent on a signaling pathway involving the transcriptional regulator YAP1. Specifically, we found that YAP1 and the transcription factor TBX5 form a complex with β-catenin. Phosphorylation of YAP1 by the tyrosine kinase YES1 leads to localization of this complex to the promoters of antiapoptotic genes, including BCL2L1 and BIRC5. A small-molecule inhibitor of YES1 impeded the proliferation of β-catenin-dependent cancers in both cell lines and animal models. These observations define a β-catenin-YAP1-TBX5 complex essential to the transformation and survival of β-catenin-driven cancers.
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“Second, YAP collaborates with other transcription regulators to alter gene expression, for example, in colon cancer cell lines YAP1, β-catenin and TBX5 transcriptional complex regulate (TCFor TEAD-independent) target genes (72).”
From A Tumour-Specific Molecular Network Promotes Tumour Growth in Drosophila by Enforcing a JNK-YKI Feedforward Loop (2023) · cites this paper as [72]
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“Conversely, overexpression of TEAD1 (Fig. 2D; Supplementary Fig. 2D), WWTR1 (Fig. 2E; Supplementary Fig. 2E), YAP1 (Fig. 2F; Supplementary Fig. 2F), or a constitutively active, nucleus-restricted form of YAP1 (38), YAP S6A (Fig. 2G; left panel; Supplementary Fig. 2G) in “KCL” cells (derived from KRAS G12C ;Stk11-/-mice; see Methods) caused drug resistance.”
From Genome-Wide CRISPR Screens Identify Multiple Synthetic Lethal Targets That Enhance KRASG12C Inhibitor Efficacy (2023) · cites this paper as [38]
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Metadata
- Authors
- Rosenbluh, J., Nijhawan, D., Cox, A. G., Li, X., Neal, J. T., Schafer, E. J., Zack, T. I., Wang, X., Tsherniak, A., Schinzel, A. C., Shao, D. D., Schumacher, S. E., Weir, B. A., Vazquez, F., Cowley, G. S., Root, D. E., Mesirov, J. P., Beroukhim, R., Kuo, C. J., Goessling, W., & Hahn, W. C.
- Affiliations
- Broad Institute (US)
- Brigham and Women's Hospital (US)
- Stanford Medicine (US)
- Corresponding author
- Hahn, William C.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2012-12
- Volume
- 151
- Issue
- 7
- Pages
- 1457-1473
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC3530160
- OpenAlex
- W2085039090
- Cited by
- 757
- References
- 71
- Citations by year
- 2026: 21 · 2025: 41 · 2024: 49 · 2023: 49 · 2022: 59 · 2021: 71 · 2020: 69 · 2019: 62 · 2018: 77 · 2017: 58 · 2016: 57 · 2015: 70 · 2014: 37 · 2013: 35 · 2012: 1
- FWCI
- 21.65
- Type
- journal article
- Language
- en
- Update notices
- erratum (2013-03-28)
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 385 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (P50CA127003, RC2CA148268, U01CA151920, R01CA140545, R01CA109467, U54CA112962, U54CA143798)
- National Institute of General Medical Sciences (T32GM007753, F32GM090437, R01GM074024)
- National Institute of Diabetes and Digestive and Kidney Diseases (U24DK085532, R01DK085720, U01DK085527, R01DK090311, U01DK085532)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
- Keywords
- β-catenin, YAP, TBX5, Wnt/β-catenin signaling, colon cancer, tumor cell survival, carcinogenesis, YES1, Bcl-xL, survivin, anti-apoptotic genes, transcriptional complex, small molecule inhibitors, cancer cell lines
- MeSH terms
- Survivin, YAP-Signaling Proteins, Animals, Cell Transformation, Neoplastic, Colon, Colonic Neoplasms, Humans, Mice, Nude, Phosphoproteins, Transcription Factors, Transcription, Genetic, Zebrafish, src-Family Kinases, T-Box Domain Proteins, Cell Line, Tumor, Adaptor Proteins, Signal Transducing, bcl-X Protein, Inhibitor of Apoptosis Proteins, beta Catenin, Mice, Proto-Oncogene Proteins c-yes
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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.
What counts as a claim ›How we measure confidence ›How we check this ›
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