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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]
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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]
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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
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Items 101–200 of 753
RAS mutations in human cancers: Roles in precision medicine
Murugan, A. K., Grieco, M., & Tsuchida, N. (2019) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2019.06.007 · Cited by 146
Src Inhibits the Hippo Tumor Suppressor Pathway through Tyrosine Phosphorylation of Lats1
Si, Y., Ji, X., Cao, X., Dai, X., Xu, L., Zhao, H., Guo, X., Yan, H., Zhang, H., Zhu, C., et al. (2017) · Cancer Research · doi:10.1158/0008-5472.can-17-0391 · Cited by 142
The regulation and function of YAP transcription co-activator
Zhu, C., Li, L., & Zhao, B. (2014) · Acta Biochimica et Biophysica Sinica · doi:10.1093/abbs/gmu110 · Cited by 143
García-Rendueles, M. E. R., Ricarte‐Filho, J. C., Untch, B. R., Landa, I., Knauf, J. A., Voza, F. A., Smith, V. E., Ganly, I., Taylor, B. S., Persaud, Y., et al. (2015) · Cancer Discovery · doi:10.1158/2159-8290.cd-15-0330 · Cited by 139
Rozengurt, E., Sinnett‐Smith, J. W., & Eibl, G. (2018) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-017-0005-2 · Cited by 137
Pan‐cancer survey of epithelial–mesenchymal transition markers across the Cancer Genome Atlas
Gibbons, D. L., & Creighton, C. J. (2017) · Developmental Dynamics · doi:10.1002/dvdy.24485 · Cited by 128
Nussinov, R., Jang, H., Tsai, C., & Cheng, F. (2019) · PLoS Computational Biology · doi:10.1371/journal.pcbi.1006658 · Cited by 134
Mechanical Control of Epithelial-to-Mesenchymal Transitions in Development and Cancer
Przybyla, L., Muncie, J. M., & Weaver, V. M. (2016) · Annual Review of Cell and Developmental Biology · doi:10.1146/annurev-cellbio-111315-125150 · Cited by 123
Xia, H., Dai, X., Yu, H., Zhou, S., Fan, Z., Wei, G., Tang, Q., Gong, Q., & Bi, F. (2018) · Cell Death and Disease · doi:10.1038/s41419-018-0302-x · Cited by 124
Modulation of the proteostasis network promotes tumor resistance to oncogenic KRAS inhibitors
Lv, X., Lu, X., Cao, J., Luo, Q., Ding, Y., Peng, F., Pataer, A., Lu, D., Han, D., Malmberg, E., et al. (2023) · Science · doi:10.1126/science.abn4180 · Cited by 123
Self-citationSong, C., Li, Y., Mou, H., Moore, J. E., Park, A., Pomyen, Y., Hough, S. H., Kennedy, Z., Fischer, A. H., Yin, H., et al. (2016) · Gastroenterology · doi:10.1053/j.gastro.2016.12.002 · Cited by 124
Self-citationHedgehog regulates yes‐associated protein 1 in regenerating mouse liver
Swiderska‐Syn, M., Xie, G., Michelotti, G. A., Jewell, M. L., Premont, R. T., Syn, W., & Diehl, A. M. (2016) · Hepatology · doi:10.1002/hep.28542 · Cited by 121
Lee, J. E., Park, H. S., Lee, D., Yoo, G., Kim, T., Jeon, H., Yeo, M., Lee, C. S., Moon, J. Y., Jung, S. S., et al. (2016) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2016.04.089 · Cited by 119
Self-citationYAP and TAZ in Lung Cancer: Oncogenic Role and Clinical Targeting
Sardo, F. L., Strano, S., & Blandino, G. (2018) · Cancers · doi:10.3390/cancers10050137 · Cited by 124
Opposing activities of the Ras and Hippo pathways converge on regulation of YAP protein turnover
Hong, X., Nguyen, H. T., Chen, Q., Zhang, R., Hagman, Z., Voorhoeve, P. M., & Cohen, S. M. (2014) · The EMBO Journal · doi:10.15252/embj.201489385 · Cited by 121
Abali, G. K., Alptekin, A., Lewis, M. S., Garraway, I. P., & Cinar, B. (2015) · Nature Communications · doi:10.1038/ncomms9126 · Cited by 121
YAP promotes erlotinib resistance in human non-small cell lung cancer cells
Hsu, P., You, B., Yang, Y., Zhang, W., Wang, Y., Xu, Z., Dai, Y., Liu, S., Yang, C., Li, H., et al. (2016) · Oncotarget · doi:10.18632/oncotarget.10458 · Cited by 121
Serresi, M., Gargiulo, G., Proost, N., Siteur, B., Cesaroni, M., Koppens, M. A. J., Xie, H., Sutherland, K. D., Hulsman, D., Citterio, E., et al. (2016) · Cancer Cell · doi:10.1016/j.ccell.2015.12.006 · Cited by 118
Zhou, Y. M., Wang, Y., Zhou, W., Chen, T., Wu, Q., Chutturghoon, V. K., Lin, B., Geng, L., Yang, Z., Zhou, L., et al. (2019) · Cancer Cell International · doi:10.1186/s12935-019-0898-7 · Cited by 118
Mechanisms of Resistance to KRASG12C Inhibitors
Dunnett-Kane, V., Nicola, P. A., Blackhall, F. H., & Lindsay, C. R. (2021) · Cancers · doi:10.3390/cancers13010151 · Cited by 122
Mutant KRAS as a critical determinant of the therapeutic response of colorectal cancer
Knickelbein, K., & Zhang, L. (2014) · Genes & Diseases · doi:10.1016/j.gendis.2014.10.002 · Cited by 124
Extracellular fluid viscosity enhances liver cancer cell mechanosensing and migration
Gonzalez‐Molina, J., Zhang, X., Borghesan, M., da Silva, J. M., Awan, M., Fuller, B. J., Gavara, N., & Selden, C. (2018) · Biomaterials · doi:10.1016/j.biomaterials.2018.05.058 · Cited by 115
Epithelial and stromal co-evolution and complicity in pancreatic cancer
Hingorani, S. R. (2023) · Nature Reviews Cancer · doi:10.1038/s41568-022-00530-w · Cited by 108
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Kim, T., Hwang, D., Lee, D., Kim, J., Kim, S., & Lim, D. (2017) · The EMBO Journal · doi:10.15252/embj.201695137 · Cited by 114
Self-citationHistological grading in colorectal cancer: new insights and perspectives.
Barresi, V., Bonetti, L. R., Ieni, A., Caruso, R. A., & Tuccari, G. (2015) · PubMed · doi:10.14670/hh-11-633 · Cited by 114
Role of the Hippo Pathway in Fibrosis and Cancer
Kim, C.-L., Choi, S.-H., & Mo, J. (2019) · Cells · doi:10.3390/cells8050468 · Cited by 114
Qiao, K., Liu, Y., Xu, Z., Zhang, H., Zhang, H., Zhang, C., Chang, Z., Lu, X., Li, Z., Luo, C., et al. (2020) · Angiogenesis · doi:10.1007/s10456-020-09744-8 · Cited by 111
Dubois, F., Keller, M., Calvayrac, O., Soncin, F., Hoa, L., Hergovich, A., Parrini, M., Mazières, J., Vaisse-Lesteven, M., Camonis, J., et al. (2016) · Cancer Research · doi:10.1158/0008-5472.can-15-1008 · Cited by 110
Substrate mechanics controls adipogenesis through YAP phosphorylation by dictating cell spreading
Cruz, J. O. L., Nardone, G., Vrbský, J., Pompeiano, A., Perestrelo, A. R., Capradossi, F., Melajová, K., Filipenský, P., & Forte, G. (2019) · Biomaterials · doi:10.1016/j.biomaterials.2019.03.009 · Cited by 111
The bad seed: Cancer stem cells in tumor development and resistance
Koren, E., & Fuchs, Y. (2016) · Drug Resistance Updates · doi:10.1016/j.drup.2016.06.006 · Cited by 112
STAT3 integrates cooperative Ras and TGF-β signals that induce Snail expression
Saitoh, M., Endo, K., Furuya, S., Minami, M., Fukasawa, A., Imamura, T., & Miyazawa, K. (2015) · Oncogene · doi:10.1038/onc.2015.161 · Cited by 106
The mammalian Hippo pathway: regulation and function of YAP1 and TAZ
Kodaka, M., & Hata, Y. (2014) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-014-1742-9 · Cited by 115
A ZEB1-miR-375-YAP1 pathway regulates epithelial plasticity in prostate cancer
Selth, L. A., Das, R., Townley, S. L., Coutinho, I., Hanson, A. R., Centenera, M. M., Stylianou, N., Sweeney, K. G., Soekmadji, C., Jovanovic, L., et al. (2016) · Oncogene · doi:10.1038/onc.2016.185 · Cited by 106
The roles of the Hippo pathway in cancer metastasis
van Rensburg, H. J. J., & Yang, X. (2016) · Cellular Signalling · doi:10.1016/j.cellsig.2016.08.004 · Cited by 109
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Ghiso, E., Migliore, C., Ciciriello, V., Morando, E., Petrelli, A., Corso, S., Luca, E. D., Gatti, G., Volante, M., & Giordano, S. (2017) · Neoplasia · doi:10.1016/j.neo.2017.10.003 · Cited by 101
A miR-130a-YAP positive feedback loop promotes organ size and tumorigenesis
Shen, S., Guo, X., Yan, H., Lu, Y., Ji, X., Li, L., Liang, T., Zhou, D., Feng, X., Zhao, J. C., et al. (2015) · Cell Research · doi:10.1038/cr.2015.98 · Cited by 104
Pancreatic cancer: Current research and future directions
Falasca, M., Kim, M., & Casari, I. (2016) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/j.bbcan.2016.01.001 · Cited by 101
Dong, X., Yang, Z., Yang, H., Li, D., & Qiu, X. (2020) · Frontiers in Oncology · doi:10.3389/fonc.2020.00160 · Cited by 101
Role of YAP/TAZ transcriptional regulators in resistance to anti-cancer therapies
Kim, M. H., & Kim, J. (2016) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-016-2412-x · Cited by 102
Self-citationDietrich, P., Koch, A., FRITZ, V. K., Hartmann, A., Bosserhoff, A., & Hellerbrand, C. (2017) · Gut · doi:10.1136/gutjnl-2017-315402 · Cited by 99
Wang, Z., Hausmann, S., Lyu, R., Li, T., Lofgren, S., Flores, N. M., Fuentes, M. E., Caporicci, M., Yang, Z., Meiners, M. J., et al. (2020) · Cancer Cell · doi:10.1016/j.ccell.2020.04.014 · Cited by 98
Resistance is futile: overcoming resistance to targeted therapies in lung adenocarcinoma
Neel, D. S., & Bivona, T. G. (2017) · npj Precision Oncology · doi:10.1038/s41698-017-0007-0 · Cited by 98
The EMT spectrum and therapeutic opportunities
Voon, D. C., Huang, R. Y., Jackson, R. A., & Thiery, J. P. (2017) · Molecular Oncology · doi:10.1002/1878-0261.12082 · Cited by 99
EMT and Stemness—Key Players in Pancreatic Cancer Stem Cells
Rodríguez-Aznar, E., Wiesmüller, L., Sáinz, B., & Hermann, P. C. (2019) · Cancers · doi:10.3390/cancers11081136 · Cited by 99
Zhou, Y., Liang, C., Xue, F., Chen, W., Zhi, X., Feng, X., Bai, X., & Liang, T. (2015) · Oncotarget · doi:10.18632/oncotarget.3585 · Cited by 97
Morvaridi, S., Dhall, D., Greene, M. I., Pandol, S. J., & Wang, Q. (2015) · Scientific Reports · doi:10.1038/srep16759 · Cited by 98
YAP and TAZ are essential for basal and squamous cell carcinoma initiation
Debaugnies, M., Sánchez‐Danés, A., Rorive, S., Raphaël, M., Liagre, M., Parent, M.-A., Brisebarre, A., Salmon, I. J., & Blanpain, C. (2018) · EMBO Reports · doi:10.15252/embr.201845809 · Cited by 96
Stiff substrates increase YAP-signaling-mediated matrix metalloproteinase-7 expression
Nukuda, A., Sasaki, C., Ishihara, S., Mizutani, T., Nakamura, K., Ayabe, T., Kawabata, K., & Haga, H. (2015) · Oncogenesis · doi:10.1038/oncsis.2015.24 · Cited by 103
Adachi, Y., Kimura, R., Hirade, K., Yanase, S., Nishioka, Y., Kasuga, N., Yamaguchi, R., & Ebi, H. (2023) · Nature Cancer · doi:10.1038/s43018-023-00575-2 · Cited by 93
A New View of Pathway-Driven Drug Resistance in Tumor Proliferation
Nussinov, R., Tsai, C., & Jang, H. (2017) · Trends in Pharmacological Sciences · doi:10.1016/j.tips.2017.02.001 · Cited by 94
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Zinatizadeh, M. R., Miri, S. R., Zarandi, P. K., Chalbatani, G. M., Rapôso, C., Mirzaei, H. R., Akbari, M. E., & Mahmoodzadeh, H. (2019) · Genes & Diseases · doi:10.1016/j.gendis.2019.11.003 · Cited by 98
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Maugeri‐Saccà, M., Barba, M., Pizzuti, L., Vici, P., Lauro, L. D., Dattilo, R., Vitale, I., Bartucci, M., Mottolese, M., & Maria, R. D. (2015) · Expert Reviews in Molecular Medicine · doi:10.1017/erm.2015.12 · Cited by 94
Pefani, D., Latusek, R., Pires, I. M., Grawenda, A. M., Yee, K. S. Y., Hamilton, G., van der Weyden, L., Esashi, F., Hammond, E. M., & O’Neill, E. E. (2014) · Nature Cell Biology · doi:10.1038/ncb3035 · Cited by 93
YAP and TAZ Take Center Stage in Cancer
Zhang, K., Qi, H.-X., Hu, Z., Chang, Y., Shi, Z., Han, X., Han, Y., Zhang, R., Zhang, Z., Chen, T., et al. (2015) · Biochemistry · doi:10.1021/acs.biochem.5b01014 · Cited by 94
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Bristol, J. A., Djavadian, R., Albright, E. R., Coleman, C. B., Ohashi, M., Hayes, M., Romero-Masters, J. C., Barlow, E. A., Farrell, P. J., Rochford, R. A., et al. (2018) · PLoS Pathogens · doi:10.1371/journal.ppat.1007179 · Cited by 94
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Baroja, I., Kyriakidis, N. C., Halder, G. A., & Moya, I. M. (2024) · Nature Communications · doi:10.1038/s41467-024-46531-1 · Cited by 96
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Sistigu, A., Modugno, F. D., Manic, G., & Nisticò, P. (2017) · Cytokine & Growth Factor Reviews · doi:10.1016/j.cytogfr.2017.05.008 · Cited by 100
Li, Y., Sun, C., Tan, Y., Zhang, H., Li, Y., & Zou, H. (2021) · International Journal of Biological Sciences · doi:10.7150/ijbs.52319 · Cited by 94
Synthetic Lethal Vulnerabilities in KRAS-Mutant Cancers
Aguirre, A. J., & Hahn, W. C. (2018) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a031518 · Cited by 90
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Rybinski, B., & Yun, K. (2016) · Oncotarget · doi:10.18632/oncotarget.11875 · Cited by 95
Raj, N., & Bam, R. (2019) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2019.00159 · Cited by 94
Ebrahimi, N., Adelian, S., Shakerian, S., Afshinpour, M., Chaleshtori, S. R., Ravari, N. R., Rezaei‐Tazangi, F., Beiranvand, S., Hamblin, M. R., & Aref, A. R. (2022) · Cytokine & Growth Factor Reviews · doi:10.1016/j.cytogfr.2022.01.006 · Cited by 91
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Fearing, B. V., Jing, L., Barcellona, M. N., Est-Witte, S. E., Buchowski, J. M., Zebala, L. P., Kelly, M. P., Luhmann, S. J., Gupta, M. C., Pathak, A., et al. (2019) · The FASEB Journal · doi:10.1096/fj.201802725rrr · Cited by 93
Atkins, M., Potier, D., Romanelli, L., Jacobs, J., Mach, J., Hamaratoglu, F., Aerts, S., & Halder, G. (2016) · Current Biology · doi:10.1016/j.cub.2016.06.035 · Cited by 88
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Yu, S., Zhang, Y., Li, Q., Zhang, Z., Zhao, G., & Xu, J. (2019) · Cell Death and Disease · doi:10.1038/s41419-019-2168-y · Cited by 88
Huang, Q., Wang, Y., Chen, X., Wang, Y., Li, Z., Du, S., Wang, L., & Chen, S. (2017) · Nanotheranostics · doi:10.7150/ntno.22091 · Cited by 88
Mokhtari, R. B., Ashayeri, N., Baghaie, L., Sambi, M., Satari, K., Baluch, N., Bosykh, D. A., Szewczuk, M. R., & Chakraborty, S. (2023) · Cancers · doi:10.3390/cancers15133468 · Cited by 92
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Kang, W. (2016) · World Journal of Gastroenterology · doi:10.3748/wjg.v22.i3.1279 · Cited by 86
Yan, H., Li, H., Silva, M. A., Guan, Y., Yang, L., Zhu, L., Zhang, Z., Li, G., & Ren, C. (2019) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-019-1356-z · Cited by 86
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Juan, W. C., & Hong, W. (2016) · Genes · doi:10.3390/genes7090055 · Cited by 88
Regulation of localization and function of the transcriptional co-activator YAP by angiomotin
Moleirinho, S., Hoxha, S., Mandati, V., Curtale, G., Troutman, S. A., Ehmer, U., & Kissil, J. L. (2017) · eLife · doi:10.7554/elife.23966 · Cited by 86
RUNX3 is a novel negative regulator of oncogenic TEAD–YAP complex in gastric cancer
Qiao, Y., Lin, S., Chen, Y., Voon, D. C., Zhu, F., Chuang, L. S. H., Wang, T., Tan, P. B. O., Lee, S. C., Yeoh, K. G., et al. (2015) · Oncogene · doi:10.1038/onc.2015.338 · Cited by 85
eIF5A-PEAK1 Signaling Regulates YAP1/TAZ Protein Expression and Pancreatic Cancer Cell Growth
Strnádel, J., Choi, S., Fujimura, K., Wang, H., Zhang, W., Wyse, M. M., Wright, T., Gross, E. T. E., Peinado, C. D., Park, H. W., et al. (2017) · Cancer Research · doi:10.1158/0008-5472.can-16-2594 · Cited by 84
Zhang, B., Zhang, Y., Zhang, J., Liu, P., Jiao, B., Wang, Z., & Ren, R. (2021) · Advanced Science · doi:10.1002/advs.202100250 · Cited by 83
Murakami, S., Nemazanyy, I., White, S. M., Chen, H., Nguyen, C. D. K., Graham, G. T., Saur, D., Pende, M., & Yi, C. (2019) · Developmental Cell · doi:10.1016/j.devcel.2019.07.022 · Cited by 83
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Addeo, A., Banna, G. L., & Friedlaender, A. (2021) · Cancers · doi:10.3390/cancers13112541 · Cited by 85
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Frittoli, E., Palamidessi, A., Iannelli, F., Zanardi, F., Villa, S., Barzaghi, L., Abdo, H., Cancila, V., Beznoussenko, G. V., Chiara, G. D., et al. (2022) · Nature Materials · doi:10.1038/s41563-022-01431-x · Cited by 91
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Klomp, J. E., Diehl, J. N., Klomp, J. A., Edwards, A. C., Yang, R., Morales, A. J., Taylor, K. E., Drizyte-Miller, K., Bryant, K. L., Schaefer, A., et al. (2024) · Science · doi:10.1126/science.adk0850 · Cited by 83
Oncofetal reprogramming drives phenotypic plasticity in WNT-dependent colorectal cancer
Mzoughi, S., Schwarz, M. C., Wang, X., Demircioğlu, D., Ulukaya, G. B., Mohammed, K., Zorgati, H., Torre, D., Tomalin, L. E., Tullio, F. D., et al. (2025) · Nature Genetics · doi:10.1038/s41588-024-02058-1 · Cited by 88
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Qi, Y., Yu, J. Q., Han, W., Fan, X., Qian, H., Wei, H. Y., Tsai, Y.-H. S., Zhao, J., Zhang, W., Liu, Q., et al. (2016) · Nature Communications · doi:10.1038/ncomms11840 · Cited by 85
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Silva, E. C. D., Dontenwill, M., Choulier, L., & Lehmann, M. (2019) · Cancers · doi:10.3390/cancers11050692 · Cited by 81
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Hsu, P., Yang, C., Jablons, D. M., & You, L. (2020) · Cancers · doi:10.3390/cancers12061361 · Cited by 85
Takeda, M., Yoshida, S., Inoue, T., Sekido, Y., Hata, T., Hamabe, A., Ogino, T., Miyoshi, N., Uemura, M., Yamamoto, H., et al. (2025) · Cancers · doi:10.3390/cancers17030428 · Cited by 82
O-GlcNAcylation is required for mutant KRAS-induced lung tumorigenesis
Taparra, K., Wang, H., Malek, R., Lafargue, A., Barbhuiya, M. A., Wang, X., Simons, B. W., Ballew, M., Nugent, K., Groves, J., et al. (2018) · Journal of Clinical Investigation · doi:10.1172/jci94844 · Cited by 80
Self-citationKulkarni, M., Tan, T. Z., Sulaiman, N. B. S., Lamar, J. M., Bansal, P., Cui, J., Qiao, Y., & Ito, Y. (2018) · Oncotarget · doi:10.18632/oncotarget.24419 · Cited by 78
Jahangiri, B., Khalaj‐Kondori, M., Asadollahi, E., & Sadeghizadeh, M. (2018) · Journal of Cell Communication and Signaling · doi:10.1007/s12079-018-0471-5 · Cited by 78
Sharif, G. M., Schmidt, M. O., Yi, C., Hu, Z., Haddad, B. R., Glasgow, E. F., Riegel, A. T., & Wellstein, A. (2015) · Oncogene · doi:10.1038/onc.2015.44 · Cited by 77
JNK signaling is converted from anti- to pro-tumor pathway by Ras-mediated switch of Warts activity
Enomoto, M., Kizawa, D., Ohsawa, S., & Igaki, T. (2015) · Developmental Biology · doi:10.1016/j.ydbio.2015.05.001 · Cited by 74
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Li, H., Li, Q., Dang, K., Ma, S., Cotton, J. L., Yang, S., Zhu, L. J., DENG, A. C., Ip, Y. T., Johnson, R. L., et al. (2019) · Cell Reports · doi:10.1016/j.celrep.2019.03.021 · Cited by 77
Hippo Signaling-Mediated Mechanotransduction in Cell Movement and Cancer Metastasis
Chang, Y.-C., Wu, J.-W., Wang, C.-W., & Jang, A. C.-C. (2020) · Frontiers in Molecular Biosciences · doi:10.3389/fmolb.2019.00157 · Cited by 81
Wang, H., Lu, B., Cabrera, J. C., Zhang, Y., Yang, Z., McAllister, G., Lindeman, A., Reece-Hoyes, J. S., Tallarico, J. A., Russ, C., et al. (2016) · Journal of Biological Chemistry · doi:10.1074/jbc.m116.722967 · Cited by 79
Alveolar Differentiation Drives Resistance to KRAS Inhibition in Lung Adenocarcinoma
Li, Z., Zhuang, X., Pan, C.-H., Yan, Y., Thummalapalli, R., Hallin, J., Torborg, S., Singhal, A., Chang, J. C., Manchado, E., et al. (2024) · Cancer Discovery · doi:10.1158/2159-8290.cd-23-0289 · Cited by 74
Alternate RASSF1 Transcripts Control SRC Activity, E-Cadherin Contacts, and YAP-Mediated Invasion
Vlahov, N., Scrace, S., Soto, M. S., Grawenda, A. M., Bradley, L., Paňková, D., Papaspyropoulos, A., Yee, K. S. Y., Buffa, F. M., Goding, C. R., et al. (2015) · Current Biology · doi:10.1016/j.cub.2015.09.072 · Cited by 79
Clonality and Evolutionary History of Rhabdomyosarcoma
Chen, L., Shern, J. F., Wei, J. S., Yohe, M. E., Song, Y., Hurd, L., Liao, H., Catchpoole, D. R., Skapek, S. X., Barr, F. G., et al. (2015) · PLoS Genetics · doi:10.1371/journal.pgen.1005075 · Cited by 77
Role of cancer-associated fibroblasts in invasion and metastasis of gastric cancer
Yu, Y. H. (2015) · World Journal of Gastroenterology · doi:10.3748/wjg.v21.i33.9717 · Cited by 78
YAP1 enhances cell proliferation, migration, and invasion of gastric cancer in vitro and in vivo
Sun, D., Li, X.-T., He, Y., Li, W., Wang, Y., Wang, H., Jiang, S., & Xin, Y. (2016) · Oncotarget · doi:10.18632/oncotarget.13188 · Cited by 76
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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