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KRAS and YAP1 Converge to Regulate EMT and Tumor Survival
Open accessAbstract
Cancer cells that express oncogenic alleles of RAS typically require sustained expression of the mutant allele for survival, but the molecular basis of this oncogene dependency remains incompletely understood. To identify genes that can functionally substitute for oncogenic RAS, we systematically expressed 15,294 open reading frames in a human KRAS-dependent colon cancer cell line engineered to express an inducible KRAS-specific shRNA. We found 147 genes that promoted survival upon KRAS suppression. In particular, the transcriptional coactivator YAP1 rescued cell viability in KRAS-dependent cells upon suppression of KRAS and was required for KRAS-induced cell transformation. Acquired resistance to Kras suppression in a Kras-driven murine lung cancer model also involved increased YAP1 signaling. KRAS and YAP1 converge on the transcription factor FOS and activate a transcriptional program involved in regulating the epithelial-mesenchymal transition (EMT). Together, these findings implicate transcriptional regulation of EMT by YAP1 as a significant component of oncogenic RAS signaling.
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“For instance, a complex consisting of YAP, TAZ, TEADs, and AP-1 (dimer of cFos and transcription factor Jun [JUN] families) was found to synergistically regulate the transcription of target genes (35–37).”
From YAP/TAZ mediates resistance to KRAS inhibitors through inhibiting proapoptosis and activating the SLC7A5/mTOR axis (2024) · cites this paper as [37]
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
“Previous studies have demonstrated that activated Yap, through genetic amplification of YAP- or WNT5a-mediated dysregulation of the Hippo pathway, enables bypass of Kras suppression in Kras-driven murine pancreatic cancer and lung cancer models (37–39).”
From YAP/TAZ mediates resistance to KRAS inhibitors through inhibiting proapoptosis and activating the SLC7A5/mTOR axis (2024) · cites this paper as [37]
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.
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“YAP, a pivotal EMT regulator gene, can restore oncogenicity in murine tumors that have lost KRAS [54,131].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [131]
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“Prior studies using inducible suppression of KRAS via RNA interference or genetically engineered inducible KrasG12D alleles (i.e., “iKras” model) have suggested that amplification of YAP1 or induction of an epithelial-to-mesenchymal transition (EMT) can confer a state of RAS independence and overcome KRASG12D suppression (35–38).”
From Mechanisms of Resistance to Oncogenic KRAS Inhibition in Pancreatic Cancer (2024) · cites this paper as [35]
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“Using a genetically engineered mouse (GEM) model of PDAC driven by inducible KRASG12D, we recently demonstrated that activation of the YAP1 oncogene drives resistance to genetic inactivation of KRAS∗, a finding further confirmed in KRAS∗-driven colorectal cancer (CRC).”
From Therapeutic targeting of syndecan-1 axis overcomes acquired resistance to KRAS-targeted therapy in gastrointestinal cancers (2025) · cites this paper as [10]
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“The YAP1 oncogene has been well established as one of the major drivers of bypassing oncogene addiction and promoting acquired resistance to targeted therapies in several cancer types, including pancreatic cancer, lung cancer, colorectal cancer, melanoma, and glioblastoma.9,10,38,39,40”
From Therapeutic targeting of syndecan-1 axis overcomes acquired resistance to KRAS-targeted therapy in gastrointestinal cancers (2025) · cites this paper as [10]
Experimental — accuracy not yet measuredIn the citing paper
“In the context of pancreatic cancer, KRAS dependency can be by-passed by the elevated expression of the transcription factor YAP1, which promotes EMT and confers cell-intrinsic resistance to KRAS loss (84, 85).”
From KRAS mutation in pancreatic cancer (2021) · cites this paper as [84]
In the citing paper
“On the one hand, it is known that YAP activity is positively correlated with the resistance to therapies targeting KRAS signaling components including RAF and MEK,[ 28, 46 ] and YAP is required for KRAS‐dependent cell transformation: extracellular supplementation of YAP activators can rescue cancer cell killing after KRAS knockdown.[ 47 ]”
From Focal Adhesion Kinase (FAK) Inhibition Synergizes with KRAS G12C Inhibitors in Treating Cancer through the Regulation of the FAK–YAP Signaling (2021) · cites this paper as [47]
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Metadata
- Authors
- Shao, D. D., Xue, W., Krall, E. B., Bhutkar, A., Piccioni, F., Wang, X., Schinzel, A. C., Sood, S., Rosenbluh, J., Kim, J. W., Zwang, Y., Roberts, T. M., Root, D. E., Jacks, T., & Hahn, W. C.
- Affiliations
- Broad Institute (US)
- Koch Institute for Integrative Cancer Research At MIT (US)
- Dana-Farber Cancer Institute (US)
- Corresponding author
- Jacks, Tyler
- Hahn, William C.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2014-07
- Volume
- 158
- Issue
- 1
- Pages
- 171-184
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC4110062
- OpenAlex
- W2064644124
- Cited by
- 744
- References
- 69
- Citations by year
- 2026: 35 · 2025: 46 · 2024: 50 · 2023: 56 · 2022: 59 · 2021: 58 · 2020: 82 · 2019: 68 · 2018: 58 · 2017: 73 · 2016: 75 · 2015: 61 · 2014: 22
- FWCI
- 38.34
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- DSpace@MIT (Massachusetts Institute of Technology) (submittedVersion, cc-by-nc-nd)
- PMC
- Funders
- U.S. Department of Defense (P30-CA14051, W81XWH)
- Howard Hughes Medical Institute
- American Association for Cancer Research
- Hope Funds for Cancer Research (HFCR-11-03-03)
- Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology (P30-CA14051)
- National Institutes of Health (W81XWH)
- National Cancer Institute (P50CA127003, K99CA169512, R01CA140545, CA14051, R00CA169512, P01CA050661, U01CA176058, P01CA154303, P30CA014051, P30-CA-14051)
- National Institute of General Medical Sciences (T32GM007753)
- 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 › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Keywords
- KRAS, YAP, oncogenic Ras, epithelial-mesenchymal transition, tumor cell survival, FOS, transcriptional coactivator, acquired drug resistance, colon cancer, lung cancer, cell transformation, transcriptional regulation
- MeSH terms
- YAP-Signaling Proteins, Animals, Cell Survival, Colonic Neoplasms, Humans, Lung Neoplasms, Phosphoproteins, Proto-Oncogene Proteins, Transcription Factors, Signal Transduction, Transcriptional Activation, Proto-Oncogene Proteins p21(ras), Drug Delivery Systems, ras Proteins, Cell Cycle Proteins, Drug Resistance, Neoplasm, HCT116 Cells, Adaptor Proteins, Signal Transducing, Mice, Epithelial-Mesenchymal Transition
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