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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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