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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.
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“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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Cites
Subramanian, A., Tamayo, P., Mootha, V. K., Mukherjee, S., Ebert, B. L., Gillette, M. A., Paulovich, A., Pomeroy, S. L., Golub, T. R., Lander, E. S., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0506580102 · Cited by 53,625
An integrated encyclopedia of DNA elements in the human genome
The ENCODE Project Consortium (2012) · Nature · doi:10.1038/nature11247 · Cited by 18,072
Trapnell, C., Williams, B. A., Pertea, G., Mortazavi, A., Kwan, G., van Baren, M. J., Salzberg, S. L., Wold, B. J., & Pachter, L. (2010) · Nature Biotechnology · doi:10.1038/nbt.1621 · Cited by 15,556
TopHat: discovering splice junctions with RNA-Seq
Trapnell, C., Pachter, L. S., & Salzberg, S. L. (2009) · Bioinformatics · doi:10.1093/bioinformatics/btp120 · Cited by 11,682
The Human Genome Browser at UCSC
Kent, W. J., Sugnet, C. W., Furey, T. S., Roskin, K. M., Pringle, T. H., Zahler, A. M., & Haussler, A. D. (2002) · Genome Research · doi:10.1101/gr.229102 · Cited by 10,400
Role of YAP/TAZ in mechanotransduction
Dupont, S., Morsut, L., Aragona, M., Enzo, E., Giulitti, S., Cordenonsi, M., Zanconato, F., Le Digabel, J., Forcato, M., Bicciato, S., et al. (2011) · Nature · doi:10.1038/nature10137 · Cited by 5,979
Zhao, B., Wei, X., Li, W., Udan, R. S., Yang, Q., Kim, J., Xie, J., Ikenoue, T., Yu, J., Li, L., et al. (2007) · Genes & Development · doi:10.1101/gad.1602907 · Cited by 3,092
Self-citationTEAD mediates YAP-dependent gene induction and growth control
Zhao, B., Ye, X., Yu, J., Li, L., Li, W., Li, S., Yu, J., Lin, J. D., Wang, C.-Y., Chinnaiyan, A. M., et al. (2008) · Genes & Development · doi:10.1101/gad.1664408 · Cited by 2,498
The Regulation of AP-1 Activity by Mitogen-activated Protein Kinases
Karin, M. (1995) · Journal of Biological Chemistry · doi:10.1074/jbc.270.28.16483 · Cited by 2,423
Creation of human tumour cells with defined genetic elements
Hahn, W. C., Counter, C. M., Lundberg, A. S., Beijersbergen, R. L., Brooks, M. W., & Weinberg, R. A. (1999) · Nature · doi:10.1038/22780 · Cited by 2,345
Self-citationThe Hippo Signaling Pathway in Development and Cancer
Pan, D. (2010) · Developmental Cell · doi:10.1016/j.devcel.2010.09.011 · Cited by 2,317
A Lentiviral RNAi Library for Human and Mouse Genes Applied to an Arrayed Viral High-Content Screen
Moffat, J., Grueneberg, D. A., Yang, X., Kim, S. Y., Kloepfer, A. M., Hinkle, G., Piqani, B., Eisenhaure, T., Luo, B., Grenier, J. K., et al. (2006) · Cell · doi:10.1016/j.cell.2006.01.040 · Cited by 1,801
Self-citationRAS oncogenes: weaving a tumorigenic web
Pylayeva-Gupta, Y., Grabocka, E., & Bar-Sagi, D. (2011) · Nature Reviews Cancer · doi:10.1038/nrc3106 · Cited by 1,789
YAP1 increases organ size and expands undifferentiated progenitor cells
Camargo, F. D., Gokhale, S., Johnnidis, J. B., Fu, D., Bell, G. W., Jaenisch, R., & Brummelkamp, T. R. (2007) · Current Biology · doi:10.1016/j.cub.2007.10.039 · Cited by 1,252
The Sp-family of transcription factors
Suske, G. (1999) · Gene · doi:10.1016/s0378-1119(99)00357-1 · Cited by 1,112
Identification and validation of oncogenes in liver cancer using an integrative oncogenomic approach
Zender, L., Spector, M. S., Xue, W., Flemming, P., Cordon-Cardo, C., Silke, J., Fan, S.-T., Luk, J. M., Wigler, M., Hannon, G. J., et al. (2006) · Cell · doi:10.1016/j.cell.2006.05.030 · Cited by 1,065
Self-citationTaube, J. H., Herschkowitz, J. I., Komurov, K., Zhou, A. Y., Gupta, S. K., Yang, J., Hartwell, K. A., Önder, T. T., Gupta, P. B., Evans, K. W., et al. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1004900107 · Cited by 1,054
Transforming properties of YAP , a candidate oncogene on the chromosome 11q22 amplicon
Overholtzer, M., Zhang, J., Smolen, G. A., Muir, B., Li, W., Sgroi, D. C., Deng, C., Brugge, J. S., & Haber, D. A. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0605579103 · Cited by 893
Essential role for oncogenic Ras in tumour maintenance
Chin, L., Tam, A., Pomerantz, J. H., Wong, M., Holash, J. A., Bardeesy, N. M., Shen, Q. “., O’Hagan, R. C., Pantginis, J., Zhou, H., et al. (1999) · Nature · doi:10.1038/22788 · Cited by 886
Conditional mouse lung cancer models using adenoviral or lentiviral delivery of Cre recombinase
DuPage, M. J. P., Dooley, A. L., & Jacks, T. (2009) · Nature Protocols · doi:10.1038/nprot.2009.95 · Cited by 873
Self-citationSingh, A., Greninger, P., Rhodes, D., Koopman, L., Violette, S., Bardeesy, N., & Settleman, J. (2009) · Cancer Cell · doi:10.1016/j.ccr.2009.03.022 · Cited by 841
Tuveson, D. A., Shaw, A. T., Willis, N. A., Silver, D. P., Jackson, E. L., Chang, S., Mercer, K. L., Grochow, R., Hock, H., Crowley, D., et al. (2004) · Cancer Cell · doi:10.1016/s1535-6108(04)00085-6 · Cited by 798
Self-citationβ-Catenin-Driven Cancers Require a YAP1 Transcriptional Complex for Survival and Tumorigenesis
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., et al. (2012) · Cell · doi:10.1016/j.cell.2012.11.026 · Cited by 757
Self-citationVassilev, A., Kaneko, K. J., Shu, H., Zhao, Y., & DePamphilis, M. L. (2001) · Genes & Development · doi:10.1101/gad.888601 · Cited by 719
Yap1 Activation Enables Bypass of Oncogenic Kras Addiction in Pancreatic Cancer
Kapoor, A., Yao, W., Ying, H., Hua, S., Liewen, A., Wang, Q., Zhong, Y., Wu, C.-J., Sadanandam, A., Hu, B., et al. (2014) · Cell · doi:10.1016/j.cell.2014.06.003 · Cited by 716
The Hippo pathway target, YAP, promotes metastasis through its TEAD-interaction domain
Lamar, J. M., Stern, P., Liu, H., Schindler, J. W., Jiang, Z.-G., & Hynes, R. O. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1212021109 · Cited by 670
Binding of Ras to Phosphoinositide 3-Kinase p110α Is Required for Ras- Driven Tumorigenesis in Mice
Gupta, S., Ramjaun, A. R., Haiko, P., Wang, Y., Warne, P. H., Nicke, B., Nye, E. L., Stamp, G., Alitalo, K. K., & Downward, J. (2007) · Cell · doi:10.1016/j.cell.2007.03.051 · Cited by 603
Fisher, G. H., Wellen, S. L., Klimstra, D., Lenczowski, J. M., Tichelaar, J. W., Lizak, M. J., Whitsett, J. A., Koretsky, A., & Varmus, H. E. (2001) · Genes & Development · doi:10.1101/gad.947701 · Cited by 582
A public genome-scale lentiviral expression library of human ORFs
Yang, X., Boehm, J. S., Yang, X., Salehi-Ashtiani, K., Hao, T., Shen, Y., Lubonja, R., Thomas, S. R., Alkan, O., Bhimdi, T., et al. (2011) · Nature Methods · doi:10.1038/nmeth.1638 · Cited by 570
Self-citationCheng, G. Z., Chan, J. L. ‐., Wang, Q., Zhang, W., Sun, C. D., & Wang, L. (2007) · Cancer Research · doi:10.1158/0008-5472.can-06-1479 · Cited by 545
Witta, S. E., Gemmill, R. M., Hirsch, F. R., Coldren, C. D., Hedman, K., Ravdel, L., Helfrich, B. A., Dziadziuszko, R., Chan, D. C. F., Sugita, M., et al. (2006) · Cancer Research · doi:10.1158/0008-5472.can-05-1988 · Cited by 524
The Hippo–YAP pathway: new connections between regulation of organ size and cancer
Zhao, B., Lei, Q., & Guan, K. (2008) · Current Opinion in Cell Biology · doi:10.1016/j.ceb.2008.10.001 · Cited by 466
Oncogene addiction: setting the stage for molecularly targeted cancer therapyPreprint
Sharma, S. V., & Settleman, J. E. (2007) · Genes & Development · doi:10.1101/gad.1609907 · Cited by 451
Zhang, J., Ji, J., Yu, M., Overholtzer, M., Smolen, G. A., Wang, R., Brugge, J. S., Dyson, N. J., & Haber, D. A. (2009) · Nature Cell Biology · doi:10.1038/ncb1993 · Cited by 438
YAP regulates neural progenitor cell number via the TEA domain transcription factorPreprint
Cao, X., Pfaff, S. L., & Gage, F. H. (2008) · Genes & Development · doi:10.1101/gad.1726608 · Cited by 412
Kajiyama, H., Shibata, K., Terauchi, M., Yamashita, M., Ino, K., Nawa, A., & Kikkawa, F. (2007) · International Journal of Oncology · doi:10.3892/ijo.31.2.277 · Cited by 410
(1994) · PubMed · Cited by 404
Ota, M., & Sasaki, H. (2008) · Development · doi:10.1242/dev.027151 · Cited by 399
Genome-scale loss-of-function screening with a lentiviral RNAi library
Root, D. E., Hacohen, N., Hahn, W. C., Lander, E. S., & Sabatini, D. M. (2006) · Nature Methods · doi:10.1038/nmeth924 · Cited by 364
Self-citationDeng, T., & Karin, M. (1994) · Nature · doi:10.1038/371171a0 · Cited by 349
c-fos is required for malignant progression of skin tumors
Sáez, E., Rutberg, S., Mueller, E., Oppenheim, H., Smoluk, J., Yuspa, S. H., & Spiegelman, B. M. (1995) · Cell · doi:10.1016/0092-8674(95)90469-7 · Cited by 346
Improved Statistical Methods for Hit Selection in High-Throughput Screening
Brideau, C., Gunter, B., Pikounis, B., & Liaw, A. I. (2003) · SLAS DISCOVERY · doi:10.1177/1087057103258285 · Cited by 337
Factors underlying sensitivity of cancers to small-molecule kinase inhibitors
Janne, P. A., Gray, N. S., & Settleman, J. (2009) · Nature Reviews Drug Discovery · doi:10.1038/nrd2871 · Cited by 312
Zuber, J., McJunkin, K., Fellmann, C., Dow, L. E., Taylor, M. J., Hannon, G., & Lowe, S. (2010) · Nature Biotechnology · doi:10.1038/nbt.1720 · Cited by 277
Regulation of Hippo Signaling by EGFR-MAPK Signaling through Ajuba Family Proteins
Reddy, B. V. V. G., & Irvine, K. D. (2013) · Developmental Cell · doi:10.1016/j.devcel.2013.01.020 · Cited by 271
Ernst Reichmann, A., Schwarz, H., Deiner, E. M., Leitner, I., Eilers, M., Berger, J., Busslinger, M., & Beug, H. (1992) · Cell · doi:10.1016/s0092-8674(05)80060-1 · Cited by 238
YAP is a candidate oncogene for esophageal squamous cell carcinoma
Muramatsu, T., Imoto, I., Matsui, T., Kozaki, K., Haruki, S., Sudol, M., Shimada, Y., Tsuda, H., Kawano, T., & Inazawa, J. (2010) · Carcinogenesis · doi:10.1093/carcin/bgq254 · Cited by 229
Transformation by ras modifies AP1 composition and activity
Mechta‐Grigoriou, F., Lallemand, D., Pfarr, C. M., & Yaniv, M. (1997) · Oncogene · doi:10.1038/sj.onc.1200900 · Cited by 212
Eger, A., Stockinger, A., Schaffhauser, B., Beug, H., & Foisner, R. (2000) · The Journal of Cell Biology · doi:10.1083/jcb.148.1.173 · Cited by 208
RalGDS is required for tumor formation in a model of skin carcinogenesis
González-Garcı́a, A., Pritchard, C. A., Paterson, H. F., Mavria, G., Stamp, G., & Marshall, C. J. (2005) · Cancer Cell · doi:10.1016/j.ccr.2005.01.029 · Cited by 181
Wang, K., Degerny, C., Xu, M., & Yang, X.-J. (2009) · Biochemistry and Cell Biology · doi:10.1139/o08-114 · Cited by 180
Lim, K.-H., & Counter, C. M. (2005) · Cancer Cell · doi:10.1016/j.ccr.2005.10.014 · Cited by 159
Response and Resistance to NF-κB Inhibitors in Mouse Models of Lung Adenocarcinoma
Xue, W., Meylan, E., Oliver, T. G., Feldser, D. M., Winslow, M. M., Bronson, R. T., & Jacks, T. (2011) · Cancer Discovery · doi:10.1158/2159-8290.cd-11-0073 · Cited by 131
Self-citationPodsypanina, K., Politi, K. A., Beverly, L. J., & VARMUS, H. E. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0801197105 · Cited by 126
Wang, Y., Ngo, V. N., Marani, M., Yang, Y., Wright, G. W., Staudt, L. M., & Downward, J. (2010) · Oncogene · doi:10.1038/onc.2010.218 · Cited by 112
Immediate-early gene activation by the MAPK pathways: what do and don't we know?
O’Donnell, A., Odrowaz, Z., & Sharrocks, A. D. (2012) · Biochemical Society Transactions · doi:10.1042/bst20110636 · Cited by 112
Mammalian Smaug Is a Translational Repressor That Forms Cytoplasmic Foci Similar to Stress Granules
Báez, M. V., & Boccaccio, G. L. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m508374200 · Cited by 110
Raf-1 Addiction in Ras-Induced Skin Carcinogenesis
Ehrenreiter, K., Kern, F., Velamoor, V., Meissl, K., Galabova‐Kovacs, G., Sibilia, M. C., & Baccarini, M. (2009) · Cancer Cell · doi:10.1016/j.ccr.2009.06.008 · Cited by 106
Nuclear localization and pro‐apoptotic signaling of YAP2 require intact PDZ‐binding motif
Oka, T., & Sudol, M. (2009) · Genes to Cells · doi:10.1111/j.1365-2443.2009.01292.x · Cited by 87
Interactions between wild-type and mutant Ras genes in lung and skin carcinogenesis
To, M. D., Rosario, R. D., Westcott, P. M. K., Banta, K. L., & Balmain, A. (2012) · Oncogene · doi:10.1038/onc.2012.404 · Cited by 82
Ledwith, B. J., Manam, S., Kraynak, A. R., Nichols, W. W., & Bradley, M. O. (1990) · Molecular and Cellular Biology · doi:10.1128/mcb.10.4.1545 · Cited by 76
The prognostic significance of epithelial-mesenchymal transition in breast cancer.
Fuchs, I. B., Lichtenegger, W., Buehler, H., Henrich, W., Stein, H., Kleine-Tebbe, A., & Schäller, G. (2002) · PubMed · Cited by 75
Jechlinger, M., Podsypanina, K., & VARMUS, H. E. (2009) · Genes & Development · doi:10.1101/gad.1801809 · Cited by 65
Wong, C. E., Yu, J. S., Quigley, D. A., To, M. D., Jen, K., Huang, P., Rosario, R. D., & Balmain, A. (2013) · Genes & Development · doi:10.1101/gad.210427.112 · Cited by 62
Non-Redundancy within the RAS Oncogene Family: Insights into Mutational Disparities in Cancer
Lau, K. S., & Haigis, K. M. (2009) · Molecules and Cells · doi:10.1007/s10059-009-0143-7 · Cited by 55
YAP1 oncogene and its eight isoforms
Sudol, M. (2012) · Oncogene · doi:10.1038/onc.2012.520 · Cited by 49
TransFind--predicting transcriptional regulators for gene sets
Kiełbasa, S. M., Klein, H., Roider, H. G., Vingron, M., & Blüthgen, N. (2010) · Nucleic Acids Research · doi:10.1093/nar/gkq438 · Cited by 36
Control of Tissue Growth and Cell Transformation by the Salvador/Warts/Hippo Pathway
Zhang, X., Grusche, F., & Harvey, K. F. (2012) · PLoS ONE · doi:10.1371/journal.pone.0031994 · Cited by 15
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Yu, F.-X., Zhao, B., & Guan, K.-L. (2015) · Cell · doi:10.1016/j.cell.2015.10.044 · Cited by 2,206
YAP/TAZ at the Roots of Cancer
Zanconato, F., Cordenonsi, M., & Piccolo, S. (2016) · Cancer Cell · doi:10.1016/j.ccell.2016.05.005 · Cited by 1,970
RAS Proteins and Their Regulators in Human Disease
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Drugging the undruggable RAS: Mission Possible?
Cox, A. D., Fesik, S. W., Kimmelman, A. C., Luo, J., & Der, C. J. (2014) · Nature Reviews Drug Discovery · doi:10.1038/nrd4389 · Cited by 1,997
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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