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Yap1 Activation Enables Bypass of Oncogenic Kras Addiction in Pancreatic Cancer
Open accessAbstract
Activating mutations in KRAS are among the most frequent events in diverse human carcinomas and are particularly prominent in human pancreatic ductal adenocarcinoma (PDAC). An inducible Kras(G12D)-driven mouse model of PDAC has established a critical role for sustained Kras(G12D) expression in tumor maintenance, providing a model to determine the potential for and the underlying mechanisms of Kras(G12D)-independent PDAC recurrence. Here, we show that some tumors undergo spontaneous relapse and are devoid of Kras(G12D) expression and downstream canonical MAPK signaling and instead acquire amplification and overexpression of the transcriptional coactivator Yap1. Functional studies established the role of Yap1 and the transcriptional factor Tead2 in driving Kras(G12D)-independent tumor maintenance. The Yap1/Tead2 complex acts cooperatively with E2F transcription factors to activate a cell cycle and DNA replication program. Our studies, along with corroborating evidence from human PDAC models, portend a novel mechanism of escape from oncogenic Kras addiction in PDAC.
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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 [38]
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
“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 [36]
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
“We had previously identified YAP1 activation, through either gene amplification or activation of a non-canonical WNT pathway, as a major driver for bypassing KRAS dependency in PDAC.9,11”
From Therapeutic targeting of syndecan-1 axis overcomes acquired resistance to KRAS-targeted therapy in gastrointestinal cancers (2025) · cites this paper as [9]
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
“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 [9]
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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“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 [9]
Experimental — accuracy not yet measured
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“Similarly, it has long been known that YAP/TAZ interact with oncogenic KRAS-mediated signaling and modulate the response to KRAS inhibition.”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [103]
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“A mesenchymal-like differentiation state can act as a resistance mechanism to KRAS inhibitors [126,128,130].”
From KRAS: Biology, Inhibition, and Mechanisms of Inhibitor Resistance (2024) · cites this paper as [130]
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“An early study of a PDAC mouse model showed that inactivation of KRAS G12D led to spontaneous tumor relapse [103].”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [103]
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“YAP1 amplification and YAP1/TEAD2 signaling enabled relapsed tumors to bypass oncogenic KRAS addiction for tumor maintenance [103].”
From Differential Response and Resistance to KRAS-Targeted Therapy (2025) · cites this paper as [103]
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“Similarly, our previous work using an inducible KrasG12D-driven PDAC model demonstrated spontaneous tumor relapse in the majority of animals following genetic extinction of KrasG12D.9”
From Therapeutic targeting of syndecan-1 axis overcomes acquired resistance to KRAS-targeted therapy in gastrointestinal cancers (2025) · cites this paper as [9]
In 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 [85]
In the citing paper
“withdrawal of mutant Ras signaling in preclinical models that include loss of tumor suppressor function leads to tumors that can re-occur in a Ras-independent fashion67.”
From Pancreatic cancer: Advances and challenges (2023) · cites this paper as [67]
In the citing paper
“some KRAS-mutant cancer cells, including lung (20) and pancreatic cancer cells (21, 22), can survive in the absence of the KRAS oncogene.”
From New Horizons in KRAS-Mutant Lung Cancer: Dawn After Darkness (2019) · cites this paper as [21]
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“Moreover, YAP can rescue cell death induced by the suppression of KRAS in cancer cells [100,101].”
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“These surviving cells were extremely enriched in tumor-initiating cells (16) and eventually were responsible for tumor relapse (19).”
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“, 2006), and recent data have revealed that YAP is essential for the progression of pancreatic ductal adenocarcinoma in Kras-mutant mice (Kapoor et al., 2014).”
BackgroundHayes, T. K., Neel, N. F., Hu, C., Gautam, P., Chénard, M., Long, B. J., Aziz, M., Kassner, M., Bryant, K. L., Pierobon, M., et al. (2015) · Cancer Cell · doi:10.1016/j.ccell.2015.11.011 · Cited by 266
“Together, our data suggest ERK and PI3K inhibitors as a potential clinically relevant combination therapy in KRAS-mutant PDAC.”
BackgroundInfluentialActin remodeling confers BRAF inhibitor resistance to melanoma cells through YAP/TAZ activation
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“In line with our results, a recently published study also demonstrated that E2F1 and YAP cooperate to enable bypass of oncogenic KRAS addiction (Kapoor et al , 2014).”
InfluentialGenomic deletion of malic enzyme 2 confers collateral lethality in pancreatic cancer
Dey, P., Baddour, J., Muller, F., Wu, C. C., Wang, H., Liao, W.-T., Lan, Z., Chen, A., Gutschner, T., Kang, Y., et al. (2017) · Nature · doi:10.1038/nature21052 · Cited by 264
Self-citationYAP/TAZ: Drivers of Tumor Growth, Metastasis, and Resistance to Therapy
Thompson, B. J. (2020) · BioEssays · doi:10.1002/bies.201900162 · Cited by 261
Regulation of TEAD Transcription Factors in Cancer Biology
Huh, H., Kim, D., Jeong, H.-S., & Park, H. (2019) · Cells · doi:10.3390/cells8060600 · Cited by 259
“TEAD2 was shown to act cooperatively with the E2F transcription factor to promote a cell-cycle gene expression program, which enabled the bypass of oncogenic KRAS addiction in PDAC and evoked KRAS-independent tumor relapse [171].”
BackgroundEpithelial memory of inflammation limits tissue damage while promoting pancreatic tumorigenesis
Poggetto, E. D., Ho, I.-L., Balestrieri, C., Yen, E.-Y., Zhang, S., Citron, F., Shah, R., Corti, D., Diaferia, G. R., Li, C.-Y., et al. (2021) · Science · doi:10.1126/science.abj0486 · Cited by 259
Self-citationTranslational advances in pancreatic ductal adenocarcinoma therapy
Hosein, A. N., Dougan, S. K., Aguirre, A. J., & Maitra, A. (2022) · Nature Cancer · doi:10.1038/s43018-022-00349-2 · Cited by 255
YAP/TAZ as master regulators in cancer: modulation, function and therapeutic approaches
Piccolo, S., Panciera, T., Contessotto, P., & Cordenonsi, M. (2022) · Nature Cancer · doi:10.1038/s43018-022-00473-z · Cited by 264
Molecular Pathogenesis of Pancreatic Cancer
Grant, T. J., Hua, K., & Singh, A. (2016) · Progress in Molecular Biology and Translational Science · doi:10.1016/bs.pmbts.2016.09.008 · Cited by 237
Metabolic networks in mutant KRAS-driven tumours: tissue specificities and the microenvironment
Kerk, S. A., Papagiannakopoulos, T. Y., Shah, Y. M., & Lyssiotis, C. A. (2021) · Nature reviews. Cancer · doi:10.1038/s41568-021-00375-9 · Cited by 246
The Hippo Pathway in Liver Homeostasis and Pathophysiology
Driskill, J. H., & Pan, D. (2020) · Annual Review of Pathology Mechanisms of Disease · doi:10.1146/annurev-pathol-030420-105050 · Cited by 236
“Many studies have identified target genes of YAP/TAZ to be those that control cell proliferation, cell migration, epithelial-mesenchymal transition, extracellular matrix organization, and cytoskeletal organization (30, 39, 40).”
BackgroundYAP Is Essential for Treg-Mediated Suppression of Antitumor Immunity
Ni, X., Tao, J., Barbi, J. J., Chen, Q., Park, B. V., Li, Z., Zhang, N., Lebid, A., Ramaswamy, A., Wei, P., et al. (2018) · Cancer Discovery · doi:10.1158/2159-8290.cd-17-1124 · Cited by 240
Disease implications of the Hippo/YAP pathway
Plouffe, S. W., Hong, A. W., & Guan, K. (2015) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2015.01.003 · Cited by 234
“A similar study found that in an inducible KRAS-driven PDAC mouse model where removal of KRAS resulted in complete tumor regression, some mice later developed spontaneous tumors due to YAP amplification and increased YAP-TEAD2 transcriptional activity [91].”
ResultSyndecan 1 is a critical mediator of macropinocytosis in pancreatic cancer
Yao, W., Rose, J. L., Wang, W., Seth, S., Jiang, H., Taguchi, A., Liu, J., Yan, L., Kapoor, A., Hou, P., et al. (2019) · Nature · doi:10.1038/s41586-019-1062-1 · Cited by 214
Self-citationPanciera, T., Citron, A., Biagio, D. D., Battilana, G., Gandin, A., Giulitti, S., Forcato, M., Bicciato, S., Panzetta, V., Fusco, S., et al. (2020) · Nature Materials · doi:10.1038/s41563-020-0615-x · Cited by 236
“Our findings offer mechanistic support to previous observations connecting YAP activity to Ras-induced tumorigenesis 23,27–29 .”
Dey, P., Li, J., Zhang, J., Chaurasiya, S., Strom, A., Wang, H., Liao, W.-T., Cavallaro, F., Denz, P., Bernard, V., et al. (2020) · Cancer Discovery · doi:10.1158/2159-8290.cd-19-0297 · Cited by 213
“On the basis of these findings, we speculated that infiltrating Th2 cells Cytokines Mediated Tumor Progression in PDAC RESEARCH ARTICLE APRIL 2020 CANCER DISCOVERY | 617 Murine T cells are predominantly CD4+ type Analysis of T-cell infiltration (iMC) GATA3+CD4+ T cells infiltrate murine PanIN Pdx1-Cre;LSL-KrasG12D scR…”
BackgroundInfluentialSelf-citationGruber, R., Panayiotou, R., Nye, E. L., Spencer‐Dene, B., Stamp, G., & Behrens, A. (2016) · Gastroenterology · doi:10.1053/j.gastro.2016.05.006 · Cited by 214
“The reliance of established PDAC tumors on KRas expression can be alleviated by up-regulation of the transcriptional regulator YAP1.(19) YAP1 has also been implicated in progression from PanIN to PDAC,(20) but its contribution at the reprogramming stage is unclear.”
BackgroundInfluentialYAP/TAZ as therapeutic targets in cancer
Zanconato, F., Battilana, G., Cordenonsi, M., & Piccolo, S. (2016) · Current Opinion in Pharmacology · doi:10.1016/j.coph.2016.05.002 · Cited by 219
“Yet, some tumors spontaneously relapse in the absence of any KRASG12D overexpression through amplification of the YAP1 locus, as such providing genetic evidence that YAPoverexpressing cellular clones are positively selected upon KRAS-inactivation [26].”
BackgroundTEAD and YAP regulate the enhancer network of human embryonic pancreatic progenitors
Cebola, I., Rodríguez‐Seguí, S. A., Cho, C. H.-H., Bessa, J., Rovira, M., Luengo, M., Chhatriwala, M., Berry, A. A., Ponsa-Cobas, J., Maestro, M. A., et al. (2015) · Nature Cell Biology · doi:10.1038/ncb3160 · Cited by 218
Yes-associated protein mediates immune reprogramming in pancreatic ductal adenocarcinoma
Murakami, S., Shahbazian, D., Surana, R., Zhang, W., Chen, H., Graham, G. T., White, S. M., Weiner, L. M., & Yi, C. (2016) · Oncogene · doi:10.1038/onc.2016.288 · Cited by 218
“Subsequent studies showed that YAP could also substitute oncogenic KRAS in promoting the growth of PDAC tumors as well as lung adenocarcinomas (Kapoor et al 2014, Shao et al 2014), and confer resistance to MAPK pathway inhibitors in KRAS or BRAF mutant tumor cells (Hugo et al 2015, Kim et al 2015,…”
BackgroundHagenbeek, T. J., Zbieg, J. R., Hafner, M., Mroue, R., Lacap, J. A., Sodir, N. M., Noland, C. L., Afghani, S., Kishore, A., Bhat, K. P., et al. (2023) · Nature Cancer · doi:10.1038/s43018-023-00577-0 · Cited by 215
Pobbati, A. V., Han, X. Y., Hung, A. W., Seetoh, W.-G., Huda, N., Chen, G.-Y., Kang, C., Chia, C. S. B., Luo, X., Hong, W., et al. (2015) · Structure · doi:10.1016/j.str.2015.09.009 · Cited by 219
“Hyperactivation of TEAD-YAP contributes to various human cancers, such as prostate cancer (Knight et al., 2008) and pancreatic cancer (Hucl et al., 2007; Kapoor et al., 2014).”
Exosome-mediated delivery of CRISPR/Cas9 for targeting of oncogenic Kras G12D in pancreatic cancer
McAndrews, K. M., Xiao, F., Chronopoulos, A., LeBleu, V. S., Kugeratski, F. G., & Kalluri, R. (2021) · Life Science Alliance · doi:10.26508/lsa.202000875 · Cited by 216
“…suggest that while inducible extinction of Kras in genetically engineered mouse models results in complete regression of pancreatic tumors in the short term, a subset of those tumors recur in the long term by escaping Kras oncogenic addiction through a YAP1-mediated transcriptional program (23).”
BackgroundTankyrase Inhibitors Target YAP by Stabilizing Angiomotin Family Proteins
Wang, W., Li, N., Li, X., Tran, M. K., Han, X., & Chen, J. (2015) · Cell Reports · doi:10.1016/j.celrep.2015.09.014 · Cited by 209
“Notably, recent studies demonstrated that YAP overexpression promoted resistance to KRAS-, RAF-, and MEK-targeted cancer therapies (Kapoor et al., 2014; Lin et al., 2015; Shao et al., 2014), highlighting the need to target YAP for cancer treatment.”
Hsu, P., Jablons, D. M., Yang, C., & You, L. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20153821 · Cited by 215
“Two studies [95,96] reported that YAP appears to take over K-ras as a cancer driver in K-ras mutant NSCLC and found that some K-ras mutant NSCLC cells relapsed after K-ras extinction without re-expression of the K-ras transgene.”
BackgroundXPO1-dependent nuclear export is a druggable vulnerability in KRAS-mutant lung cancer
Kim, J., McMillan, E., Kim, H. S., Venkateswaran, N., Makkar, G., Rodriguez-Canales, J., Villalobos, P., Neggers, J. E., Mendiratta, S., Wei, S., et al. (2016) · Nature · doi:10.1038/nature19771 · Cited by 202
Song, S., Xie, M., Scott, A. W., Jin, J., Ma, L., Dong, X., Skinner, H. D., Johnson, R. L., Ding, S., & Ajani, J. A. (2017) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-17-0560 · Cited by 205
“YAP1 also crosstalks with and activates many oncogenic signaling pathways, such as KRAS (16, 17), RhoA (18, 19), and Wnt/b-catenin (20, 21), to mediate tumor growth and therapy resistance (15, 20, 22, 23).”
BackgroundSelf-citationOTUB2 Promotes Cancer Metastasis via Hippo-Independent Activation of YAP and TAZ
Zhang, Z., Du, J., Wang, S., Shao, L., Jin, K., Li, F., Wei, B., Ding, W., Fu, P., van Dam, H., et al. (2018) · Molecular Cell · doi:10.1016/j.molcel.2018.10.030 · Cited by 195
Oncogenic Kras drives invasion and maintains metastases in colorectal cancer
Boutin, A. T., Liao, W.-T., Wang, M., Hwang, S. S., Karpinets, T. V., Cheung, H., Chu, G. C., Jiang, S., Hu, J., Chang, K., et al. (2017) · Genes & Development · doi:10.1101/gad.293449.116 · Cited by 195
“…of pathways downstream from activated KRAS (Pylayeva-Gupta et al. 2011), the existence of alternative KRAS-independent proliferation/ survival signaling pathways such as YAP (Kapoor et al. 2014), and/or the intratumoral genomic heterogeneity of the KRAS mut allele across the cancer cell population.”
Self-citationKRAS drives immune evasion in a genetic model of pancreatic cancer
Ischenko, I., D’Amico, S., Rao, M., Li, J., Hayman, M. J., Powers, S., Petrenko, O., & Reich, N. C. (2021) · Nature Communications · doi:10.1038/s41467-021-21736-w · Cited by 192
Muthalagu, N., Monteverde, T., Raffo-Iraolagoitia, X., Wiesheu, R., Whyte, D., Hedley, A., Laing, S., Kruspig, B., Upstill-Goddard, R., Shaw, R., et al. (2020) · Cancer Discovery · doi:10.1158/2159-8290.cd-19-0620 · Cited by 182
“Interestingly, cell lines that lacked increased KRASG12D allelic dosage contained amplifications of alternative oncogenes that encode proteins that may serve as potentially rate-limiting RAS effectors, including MYC, YAP1, and NF-κB (9, 14).”
BackgroundSurvival of pancreatic cancer cells lacking KRAS function
Muzumdar, M. D., Chen, P.-Y., Dorans, K. J., Chung, K. M., Bhutkar, A., Hong, E., Noll, E. M., Sprick, M. R., Trumpp, A., & Jacks, T. (2017) · Nature Communications · doi:10.1038/s41467-017-00942-5 · Cited by 177
KRAS-related proteins in pancreatic cancer
Mann, K. M., Ying, H., Juan, J. M., Jenkins, N. A., & Copeland, N. G. (2016) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2016.09.003 · Cited by 192
“Please cite this article as: Mann, K.M., et al., KRAS-related proteins in pan 10.1016/j.pharmthera.2016.09.003 The survival of these incipient tumor cells may explain the spontaneous tumor recurrence following KRAS extinction in the iKrasmodel (Kapoor et al., 2014).”
BackgroundInfluentialSelf-citationA time for YAP1: Tumorigenesis, immunosuppression and targeted therapy
Shibata, M., Ham, K., & Hoque, M. O. (2018) · International Journal of Cancer · doi:10.1002/ijc.31561 · Cited by 190
“In pancreatic cancer, YAP1 activation enables the bypass of oncogenic KRAS addiction.(62) These insights reinforce that YAP1 plays its oncogenic roles by an independent pathway from KRAS.”
BackgroundA p53 Super-tumor Suppressor Reveals a Tumor Suppressive p53-Ptpn14-Yap Axis in Pancreatic Cancer
Mello, S. S., Valente, L. J., Raj, N., Seoane, J. A., Flowers, B. M., McClendon, J., Bieging-Rolett, K. T., Lee, J., Ivanochko, D., Kozak, M. M., et al. (2017) · Cancer Cell · doi:10.1016/j.ccell.2017.09.007 · Cited by 179
“Recent studies continue to illuminate the contribution of new proteins to PDACdevelopment, such as the Yap transcriptional coactivator, which is essential for progression of preneoplastic lesions to PDAC in mouse models and can even substitute for Kras activation (Kapoor et al., 2014; Zhang et al., 2014).”
InfluentialEmerging evidence on the role of the Hippo/YAP pathway in liver physiology and cancer
Yimlamai, D., Fowl, B. H., & Camargo, F. D. (2015) · Journal of Hepatology · doi:10.1016/j.jhep.2015.07.008 · Cited by 177
“Some phenotypes include intestinal cell fate changes through Klf4 [69], enable pancreatic adenocarcinoma relapse utilizing E2F and TEAD2 [70], specifying the mouse trophectoderm in conjunction with RBP-J [71] as well as facilitating epithelial to mesenchymal transition in lung cancer through co-binding with KRAS/FOS […”
Pearson, J. D., Huang, K., Pacal, M., McCurdy, S. R., Lü, S., Aubry, A., Yu, T., Wadosky, K. M., Zhang, L., Wang, T., et al. (2021) · Cancer Cell · doi:10.1016/j.ccell.2021.06.016 · Cited by 178
“Thus, YAP suppresses YAPoff cancers through TEAD binding and gene activation, identical to the oncogenic mechanism in YAPon cancers (He et al., 2019; Kapoor et al., 2014; Ota and Sasaki, 2008).”
BackgroundSRC tyrosine kinase activates the YAP/TAZ axis and thereby drives tumor growth and metastasis
Lamar, J. M., Xiao, Y., Norton, E., Jiang, Z.-G., Gerhard, G. M., Kooner, S., Warren, J. S. A., & Hynes, R. O. (2019) · Journal of Biological Chemistry · doi:10.1074/jbc.ra118.004364 · Cited by 169
The Hippo pathway in normal development and cancer
Maugeri‐Saccà, M., & Maria, R. D. (2018) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2017.12.011 · Cited by 169
RAS Synthetic Lethal Screens Revisited: Still Seeking the Elusive Prize?
Downward, J. (2015) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-14-2180 · Cited by 168
“Recently, it has been shown that upregulation of YAP1 function can relieve KRAS oncogene addiction, and it is likely that KRAS deletion from HCT116 or DLD1 colon cancer cells will have subjected them to such a selective event (40, 41).”
BackgroundMarchetti, C., Zyner, K. G., Ohnmacht, S. A., Robson, M. P., Haider, S. M., Morton, J. P., Marsico, G., Vo, T. D., Laughlin, S., Ahmed, A. A., et al. (2018) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.7b01781 · Cited by 168
Control of stem cell renewal and fate by YAP and TAZ
Driskill, J. H., & Pan, D. (2023) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-023-00644-5 · Cited by 173
“YAP drives the recurrence of KRAS -mutant pancreatic cancer after KRAS knockdown 151 , and YAP is required in KRAS -mutant lung cancers that have grown resistant to MEK and TBK/JAK inhibitors 152 .”
BackgroundKitai, H., Ebi, H., Tomida, S., Floros, K. V., Kotani, H., Adachi, Y., Oizumi, S., Nishimura, M., Faber, A. C., & Yano, S. (2016) · Cancer Discovery · doi:10.1158/2159-8290.cd-15-1377 · Cited by 162
miR-375 is involved in Hippo pathway by targeting YAP1/TEAD4-CTGF axis in gastric carcinogenesis
Kang, W., Huang, T., Zhou, Y., Zhang, J., Lung, R. W. M., TONG, J. H. M., Chan, A. W. H., Zhang, B., Wong, C. C., Wu, F., et al. (2018) · Cell Death and Disease · doi:10.1038/s41419-017-0134-0 · Cited by 159
Self-citationChapeau, E. A., Sansregret, L., Galli, G. G., Chêne, P., Wartmann, M., Mourikis, T. P., Jaaks, P., Baltschukat, S., Barbosa, I. A. M., Bauer, D., et al. (2024) · Nature Cancer · doi:10.1038/s43018-024-00754-9 · Cited by 168
“TEAD2 paralog activation by YAP has been shown to compensate for loss of KRAS G12D activity in PDAC tumor models 5 , suggesting a benefit to co-inhibiting KRAS G12D and TEAD2.”
Tumor Microenvironment Remodeling Enables Bypass of Oncogenic KRAS Dependency in Pancreatic Cancer
Hou, P., Kapoor, A., Zhang, Q., Li, J., Wu, C.-J., Li, J., Lan, Z., Tang, M., Ma, X., Ackroyd, J. J., et al. (2020) · Cancer Discovery · doi:10.1158/2159-8290.cd-19-0597 · Cited by 154
“The iKPC cells were transfected with luciferase-mCherry reporter as described previously (17).”
BackgroundMethodInfluentialSelf-citationControl of Proliferation and Cancer Growth by the Hippo Signaling Pathway
Ehmer, U., & Sage, J. (2015) · Molecular Cancer Research · doi:10.1158/1541-7786.mcr-15-0305 · Cited by 161
“Although this method did not specifically inhibit the YAP/TEAD interaction, transcriptional programs that are likely dependent on TEAD were significantly altered in thismodel, including E2F target genes (23, 128), as well as targets of HNF4a and FOXA2 (153).”
BackgroundInfluentialChen, Y.-A., Lu, C.-Y., Cheng, T., Pan, S., Chen, H., & Chang, N. (2019) · Frontiers in Oncology · doi:10.3389/fonc.2019.00060 · Cited by 160
Chen, C., Yuan, W., Zhou, Q., Shao, B., Guo, Y., Wang, W., Yang, S., Guo, Y., Zhao, L., Dang, Q., et al. (2021) · Theranostics · doi:10.7150/thno.51342 · Cited by 153
YAP1 and its fusion proteins in cancer initiation, progression and therapeutic resistance
Szulzewsky, F., Holland, E. C., & Vasioukhin, V. I. (2021) · Developmental Biology · doi:10.1016/j.ydbio.2020.12.018 · Cited by 155
The Hippo Pathway: Immunity and Cancer
Taha, Z., van Rensburg, H. J. J., & Yang, X. (2018) · Cancers · doi:10.3390/cancers10040094 · Cited by 154
A Small Molecule with Big Impact: MRTX1133 Targets the KRASG12D Mutation in Pancreatic Cancer
Wei, D., Wang, L., Zuo, X., Maitra, A., & Bresalier, R. S. (2023) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-23-2098 · Cited by 177
Metadata
- Authors
- Kapoor, A., Yao, W., Ying, H., Hua, S., Liewen, A., Wang, Q., Zhong, Y., Wu, C.-J., Sadanandam, A., Hu, B., Chang, Q., Chu, G. C., Al-Khalil, R., Jiang, S., Xia, H., Fletcher-Sananikone, E., Lim, C., Horwitz, G. I., Viale, A., Pettazzoni, P., Sanchez, N., Wang, H., Protopopov, A., Zhang, J., Heffernan, T., Johnson, R. L., Chin, L., Wang, Y. A., Draetta, G., & DePinho, R. A.
- Affiliations
- The University of Texas MD Anderson Cancer Center (US)
- Institute of Cancer Research (GB)
- Brigham and Women's Hospital (US)
- Corresponding author
- Ying, Haoqiang
- DePinho, Ronald A.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2014-07
- Volume
- 158
- Issue
- 1
- Pages
- 185-197
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC4109295
- OpenAlex
- W2157912474
- Cited by
- 716
- References
- 59
- Citations by year
- 2026: 29 · 2025: 45 · 2024: 65 · 2023: 67 · 2022: 56 · 2021: 74 · 2020: 63 · 2019: 70 · 2018: 59 · 2017: 60 · 2016: 49 · 2015: 62 · 2014: 16
- FWCI
- 31.06
- Type
- journal article
- Language
- en
- Update notices
- erratum (2019-11-14)
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion, cc-by-nc-nd)
- Funders
- National Institute for Health and Care Research
- National Cancer Institute (CA-16672, U01CA084313, P30CA016672, P01CA117969)
- National Institute of Diabetes and Digestive and Kidney Diseases (R56DK094865, R01DK102611)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- YAP, TEAD2, KRAS G12D, pancreatic ductal adenocarcinoma, tumor recurrence, MAPK signaling, E2F transcription factors, cell cycle, DNA replication, transcriptional coactivator
- MeSH terms
- YAP-Signaling Proteins, TEA Domain Transcription Factors, Adenocarcinoma, Animals, Cell Cycle, Disease Models, Animal, DNA Replication, DNA-Binding Proteins, Humans, Pancreatic Neoplasms, Phosphoproteins, Proto-Oncogene Proteins, Transcription Factors, Proto-Oncogene Proteins p21(ras), ras Proteins, Cell Cycle Proteins, Carcinoma, Pancreatic Ductal, Cell Line, Tumor, Adaptor Proteins, Signal Transducing, E2F Transcription Factors, Mice
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