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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A complex consisting of YAP, TAZ, TEADs, and AP-1 synergistically regulates transcription of target genes.
“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]
In Results, “FOS and YAP1 coordinately regulate downstream targets” (page not supplied), the paper reports that YAP1 and FOS interact and occupy promoters of shared target genes. It does not establish a complex containing YAP, TAZ, TEADs, and AP-1 or show that such a complex synergistically regulates transcription; the same section reports no detected interaction between YAP1 and JUN. (LLM, conf=0.88)
Experimental — accuracy not yet measuredActivated 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.
“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]
The Discussion, under “Models of resistance to RAS oncogenic addiction” (page not provided), reports Yap1 amplification in relapsed murine pancreatic tumors, citing Kapoor et al. The Results, under “Yap1 mediates resistance to Kras suppression” (page not provided), show a compensatory role for Yap1 in a murine lung cancer model. Our copy does not link the lung result to YAP amplification or describe WNT5a-mediated Hippo dysregulation as a bypass mechanism. (LLM, conf=0.88)
Experimental — accuracy not yet measuredYAP can restore oncogenicity in murine tumors that have lost KRAS.
“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]
In Results, ‘Yap1 mediates resistance to Kras suppression in a KrasG12D-driven lung cancer mouse model,’ forced YAP1 expression partially prevented tumor regression after Kras suppression, and tumors later relapsed with elevated Yap1 activity. This supports a compensatory role for YAP1 in murine tumors, but the paper shows partial protection after Kras suppression, not full restoration of oncogenicity after loss of the KRAS gene. (LLM, conf=0.84)
Experimental — accuracy not yet measuredPrior studies using inducible suppression of KRAS via RNA interference or genetically engineered inducible KrasG12D alleles have suggested that amplification of YAP1 or induction of an epithelial-to-mesenchymal transition can confer a state of RAS independence and overcome KRASG12D suppression.
“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]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredActivation of YAP1 oncogene drives resistance to genetic inactivation of KRAS* in a GEM model of PDAC, confirmed in KRAS*-driven CRC.
“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]
The Results section reports that YAP1 rescued KRAS suppression in human KRAS-mutant colon cancer cell lines. But this paper's genetically engineered mouse experiment used lung cancer, not PDAC; the Discussion attributes the inducible-Kras pancreatic model to Kapoor et al. No page numbers are available in our copy. (LLM, conf=0.90)
Experimental — accuracy not yet measured
YAP1 is one of the major drivers of bypassing oncogene addiction and promoting acquired resistance to targeted therapies in several cancer types.
“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]
The Results section reports that YAP1 rescued cells from KRAS suppression in colorectal and pancreatic cancer lines; it also reports that Yap1 suppression delayed relapse in a mouse model of KRAS-driven lung cancer. This supports bypass of KRAS dependence in those settings, but the paper does not establish YAP1 as a major driver of acquired resistance to targeted therapies across the listed cancer types, including melanoma and glioblastoma. No page numbers were provided in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIn pancreatic cancer, KRAS dependency can be bypassed by elevated expression of transcription factor YAP1, which promotes EMT and confers cell-intrinsic resistance to KRAS loss.
“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]
YAP is required for KRAS-dependent cell transformation; extracellular supplementation of YAP activators can rescue cancer cell killing after KRAS knockdown.
“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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“…of KRAS via RNA interference or genetically engineered inducible Kras G12D 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 KRAS G12D suppression (35–38).”
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Crumbs3-Mediated Polarity Directs Airway Epithelial Cell Fate through the Hippo Pathway Effector Yap
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Mechanoregulation and pathology of YAP/TAZ via Hippo and non‐Hippo mechanisms
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- 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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