Hostname: page-component-848d4c4894-5nwft Total loading time: 0 Render date: 2024-05-11T19:28:08.463Z Has data issue: false hasContentIssue false
  • English
  • Français

The Hippo transducers TAZ and YAP in breast cancer: oncogenic activities and clinical implications

Published online by Cambridge University Press:  02 July 2015

Marcello Maugeri-Saccà ,
Maddalena Barba ,
Laura Pizzuti ,
Patrizia Vici ,
Luigi Di Lauro ,
Rosanna Dattilo ,
Ilio Vitale ,
Monica Bartucci ,
Marcella Mottolese  and
Ruggero De Maria
Marcello Maugeri-Saccà*
Affiliation:
Division of Medical Oncology B, Regina Elena National Cancer Institute, Rome, Italy Scientific Direction, Regina Elena National Cancer Institute, Rome, Italy
Maddalena Barba
Affiliation:
Division of Medical Oncology B, Regina Elena National Cancer Institute, Rome, Italy Scientific Direction, Regina Elena National Cancer Institute, Rome, Italy
Laura Pizzuti
Affiliation:
Division of Medical Oncology B, Regina Elena National Cancer Institute, Rome, Italy
Patrizia Vici
Affiliation:
Division of Medical Oncology B, Regina Elena National Cancer Institute, Rome, Italy
Luigi Di Lauro
Affiliation:
Division of Medical Oncology B, Regina Elena National Cancer Institute, Rome, Italy
Rosanna Dattilo
Affiliation:
Department of Hematology, Oncology and Molecular Medicine, Istituto Superiore di Sanità, Rome, Italy
Ilio Vitale
Affiliation:
Scientific Direction, Regina Elena National Cancer Institute, Rome, Italy
Monica Bartucci
Affiliation:
Rutgers Cancer Institute of New Jersey, New Brunswick, New Jersey, USA
Marcella Mottolese
Affiliation:
Department of Pathology, Regina Elena National Cancer Institute, Rome, Italy
Ruggero De Maria*
Affiliation:
Scientific Direction, Regina Elena National Cancer Institute, Rome, Italy
*
*Corresponding authors: Marcello Maugeri-Saccà, Division of Medical Oncology B and Scientific Direction, Regina Elena National Cancer Institute, Via Elio Chianesi 53, 00144 Rome, Italy. E-mail: maugeri@ifo.itRuggero De Maria, Scientific Direction, Regina Elena National Cancer Institute, Via Elio Chianesi 53, 00144 Rome, Italy. E-mail: demaria@ifo.it
*Corresponding authors: Marcello Maugeri-Saccà, Division of Medical Oncology B and Scientific Direction, Regina Elena National Cancer Institute, Via Elio Chianesi 53, 00144 Rome, Italy. E-mail: maugeri@ifo.itRuggero De Maria, Scientific Direction, Regina Elena National Cancer Institute, Via Elio Chianesi 53, 00144 Rome, Italy. E-mail: demaria@ifo.it
Get access Rights & Permissions [Opens in a new window]

Abstract

The Hippo signalling is emerging as a tumour suppressor pathway whose function is regulated by an intricate network of intracellular and extracellular cues. Defects in the signal cascade lead to the activation of the Hippo transducers TAZ and YAP. Compelling preclinical evidence showed that TAZ/YAP are often aberrantly engaged in breast cancer (BC), where their hyperactivation culminates into a variety of tumour-promoting functions such as epithelial-to-mesenchymal transition, cancer stem cell generation and therapeutic resistance. Having acquired a more thorough understanding in the biology of TAZ/YAP, and the molecular outputs they elicit, has prompted a first wave of exploratory, clinically-focused analyses aimed at providing initial hints on the prognostic/predictive significance of their expression. In this review, we discuss oncogenic activities linked with TAZ/YAP in BC, and we propose clinical strategies for investigating their role as biomarkers in the clinical setting. Finally, we address the therapeutic potential of TAZ/YAP targeting and the modalities that, in our opinion, should be pursued in order to further study the biological and clinical consequences of their inhibition.

Type
Review Article
Information
Expert Reviews in Molecular Medicine , Volume 17 , 2015 , e14
Copyright
Copyright © Cambridge University Press 2015 

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1.NCCN Clinical Practice Guidelines in Oncology: Breast Cancer, Version 3.2014. Available at: http://www.nccn.org/professionals/physician_gls/f_guidelines.asp Google Scholar
2. Perou, C.M. (2000) Molecular portraits of human breast tumours. Nature 406, 747-752 Google Scholar
3. Cancer Genome Atlas Network (2012) Comprehensive molecular portraits of human breast tumours. Nature 490, 61-70 CrossRefGoogle Scholar
4. Johnson, R. and Halder, G. (2014) The two faces of Hippo: targeting the Hippo pathway for regenerative medicine and cancer treatment. Nature Reviews Drug Discovery13, 63-79 Google Scholar
5. Justice, R.W. et al. (1995) The Drosophila tumor suppressor gene warts encodes a homolog of human myotonic dystrophy kinase and is required for the control of cell shape and proliferation. Genes & Development 9, 534-546 Google Scholar
6. Xu, T. et al. (1995) Identifying tumor suppressors in genetic mosaics: the Drosophila lats gene encodes a putative protein kinase. Development 121, 1053-1063 Google Scholar
7. Pantalacci, S. et al. (2003) The Salvador partner Hippo promotes apoptosis and cell-cycle exit in Drosophila . Nature Cell Biology 5, 921-927 Google Scholar
8. Udan, R.S. et al. (2003) Hippo promotes proliferation arrest and apoptosis in the Salvador/Warts pathway. Nature Cell Biology 5, 914-920 CrossRefGoogle ScholarPubMed
9. Wu, S. et al. (2003) Hippo encodes a Ste-20 family protein kinase that restricts cell proliferation and promotes apoptosis in conjunction with salvador and warts. Cell 114, 445-456 CrossRefGoogle ScholarPubMed
10. Jia, J. et al. (2003) The Drosophila Ste20 family kinase dMST functions as a tumor suppressor by restricting cell proliferation and promoting apoptosis. Genes & Development 17, 2514-2519 Google Scholar
11. Tapon, N. et al. (2002) Salvador Promotes both cell cycle exit and apoptosis in Drosophila and is mutated in human cancer cell lines. Cell 110, 467-478 Google Scholar
12. Harvey, K.F. (2003) The Drosophila Mst ortholog, hippo, restricts growth and cell proliferation and promotes apoptosis. Cell 114, 457-467 CrossRefGoogle ScholarPubMed
13. Hamaratoglu, F. et al. (2006) The tumour-suppressor genes NF2/Merlin and Expanded act through Hippo signalling to regulate cell proliferation and apoptosis. Nat Cell Biol 8, 27-36 Google Scholar
14. Camargo, F.D. et al. (2007) YAP1 increases organ size and expands undifferentiated progenitor cells. Current Biology 17, 2054-2060 Google Scholar
15. Zhao, B. et al. (2007) Inactivation of YAP oncoprotein by the Hippo pathway is involved in cell contact inhibition and tissue growth control. Genes & Development 21, 2747-2761 CrossRefGoogle ScholarPubMed
16. Wu, S. et al. (2008) The TEAD/TEF family protein Scalloped mediates transcriptional output of the Hippo growth-regulatory pathway. Developmental Cell 14, 388-398 Google Scholar
17. Zhang, L. et al. (2008) The TEAD/TEF family of transcription factor Scalloped mediates Hippo signaling in organ size control. Developmental Cell 14, 377-387 Google Scholar
18. Zhou, D. et al. (2009) Mst1 and Mst2 maintain hepatocyte quiescence and suppress hepatocellular carcinoma development through inactivation of the Yap1 oncogene. Cancer Cell 16, 425-438 Google Scholar
19. Fernández, B.G. et al. (2011) Actin-Capping Protein and the Hippo pathway regulate F-actin and tissue growth in Drosophila . Development 138, 2337-2346 Google Scholar
20. Sansores-Garcia, L. et al. (2011) Modulating F-actin organization induces organ growth by affecting the Hippo pathway. EMBO J 30, 2325-2335 Google Scholar
21. Harvey, K.F., Zhang, X. and Thomas, D.M. (2013) The Hippo pathway and human cancer. Nature Reviews Cancer 13, 246-257 CrossRefGoogle ScholarPubMed
22. Dong, J. et al. (2007) Elucidation of a universal size-control mechanism in Drosophila and mammals. Cell 130, 1120-1133 Google Scholar
23. Huang, J. et al. (2005) The Hippo signaling pathway coordinately regulates cell proliferation and apoptosis by inactivating Yorkie, the Drosophila homolog of YAP. Cell 122, 421-434 CrossRefGoogle ScholarPubMed
24. Lei, Q.Y. et al. (2008) TAZ promotes cell proliferation and epithelial–mesenchymal transition and is inhibited by the hippo pathway. Molecular and Cellular Biology 28, 2426-2436 CrossRefGoogle ScholarPubMed
25. Piccolo, S., Dupont, S. and Cordenonsi, M. (2014) The biology of YAP/TAZ: Hippo signaling and beyond. Physiological Reviews 94, 1287-1312 Google Scholar
26. Hong, W. and Guan, K.L. (2012) The YAP and TAZ transcription co-activators: key downstream effectors of the mammalian Hippo pathway. Seminars in Cell and Developmental Biology 23, 785-793 Google Scholar
27. Liu, C.Y. et al. (2010) The hippo tumor pathway promotes TAZ degradation by phosphorylating a phosphodegron and recruiting the SCF{beta}-TrCP E3 ligase. Journal of Biological Chemistry 285, 37159-37169 Google Scholar
28. Zhao, B. et al. (2010) A coordinated phosphorylation by Lats and CK1 regulates YAP stability through SCF(beta-TRCP). Genes & Development 24, 72-85 CrossRefGoogle ScholarPubMed
29. Dupont, S. et al. (2011) Role of YAP/TAZ in mechanotransduction. Nature 474, 179-183 Google Scholar
30. Sorrentino, G. et al. (2014) Metabolic control of YAP and TAZ by the mevalonate pathway. Nature Cell Biology 16, 357-366 CrossRefGoogle ScholarPubMed
31. Azzolin, L. et al. (2014) YAP/TAZ incorporation in the β-catenin destruction complex orchestrates the Wnt response. Cell 158, 157-170 Google Scholar
32. Bartucci, M. et al. (2015) TAZ is required for metastatic activity and chemoresistance of breast cancer stem cells. Oncogene 34, 681-690 Google Scholar
33. Vici, P. et al. (2014) The Hippo transducer TAZ as a biomarker of pathological complete response in HER2-positive breast cancer patients treated with trastuzumab-based neoadjuvant therapy. Oncotarget 5, 9619-9625 Google Scholar
34. Lehn, S. et al. (2014) Decreased expression of Yes-associated protein is associated with outcome in the luminal A breast cancer subgroup and with an impaired tamoxifen response. BMC Cancer 14, 119 Google Scholar
35. Min Kim, H. et al. (2014) Metaplastic carcinoma show different expression pattern of YAP compared to triple-negative breast cancer. Tumor Biology 36, 1207-1212 Google Scholar
36. Kim, S.K. et al. (2014) Yes-associated protein (YAP) is differentially expressed in tumor and stroma according to the molecular subtype of breast cancer. International Journal of Clinical and Experimental Pathology 7, 3224-3234 Google Scholar
37. Skibinski, A. et al. (2014) The Hippo transducer TAZ interacts with the SWI/SNF complex to regulate breast epithelial lineage commitment. Cell Reports 6, 1059-1072 Google Scholar
38. Chan, S.W. et al. (2008) A role for TAZ in migration, invasion, and tumorigenesis of breast cancer cells. Cancer Research 68, 2592-2598 Google Scholar
39. Chan, S.W. et al. (2009) TEADs mediate nuclear retention of TAZ to promote oncogenic transformation. The Journal of Biological Chemistry 284, 14347-14358 Google Scholar
40. Zhao, D., Zhi, X., Zhou, Z. and Chen, C. (2012) TAZ antagonizes the WWP1-mediated KLF5 degradation and promotes breast cell proliferation and tumorigenesis. Carcinogenesis 33, 59-67 Google Scholar
41. Habbig, S. et al. (2011) NPHP4, a cilia-associated protein, negatively regulates the Hippo pathway. The Journal of Cell Biology 193, 633-642 Google Scholar
42. Habbig, S. et al. (2012) The ciliopathy disease protein NPHP9 promotes nuclear delivery and activation of the oncogenic transcriptional regulator TAZ. Human Molecular Genetics 21, 5528-5538 Google Scholar
43. Hiemer, S.E., Szymaniak, A.D. and Varelas, X. (2014) The transcriptional regulators TAZ and YAP direct transforming growth factor β-induced tumorigenic phenotypes in breast cancer cells. Journal of Biological Chemistry 289, 13461-13474 Google Scholar
44. Overholtzer, M. et al. (2006) Transforming properties of YAP, a candidate oncogene on the chromosome 11q22 amplicon. Proceedings of the National Academy of Sciences of the United States of America 103, 12405-12410 Google Scholar
45. Wang, X., Su, L. and Ou, Q. (2012) Yes-associated protein promotes tumour development in luminal epithelial derived breast cancer. European Journal of Cancer 48, 1227-1234 CrossRefGoogle ScholarPubMed
46. Chen, Q. et al. (2014) A temporal requirement for Hippo signaling in mammary gland differentiation, growth, and tumorigenesis. Genes & Development 28, 432-437 CrossRefGoogle ScholarPubMed
47. Zhang, J. et al. (2009) YAP-dependent induction of amphiregulin identifies a non-cell-autonomous component of the Hippo pathway. Nature Cell Biology 11, 1444-1450 CrossRefGoogle ScholarPubMed
48. Yang, N. et al. (2012) TAZ induces growth factor-independent proliferation through activation of EGFR ligand amphiregulin. Cell Cycle 11, 2922-2930 CrossRefGoogle ScholarPubMed
49. Bendinelli, P. et al. (2013) Hypoxia inducible factor-1 is activated by transcriptional co-activator with PDZ-binding motif (TAZ) versus WWdomain-containing oxidoreductase (WWOX) in hypoxic microenvironment of bone metastasis from breast cancer. European Journal of Cancer 49, 2608-2618 Google Scholar
50. Lamar, J.M. et al. (2012) The Hippo pathway target, YAP, promotes metastasis through its TEAD-interaction domain. Proceedings of the National Academy of Sciences of the United States of America 109, E2441-E2450 Google ScholarPubMed
51. Chen, D. et al. (2012) LIFR is a breast cancer metastasis suppressor upstream of the Hippo-YAP pathway and a prognostic marker. Nature Medicine 18, 1511-1517 Google Scholar
52. Madar, S., Goldstein, I. and Rotter, V. (2013) ‘Cancer associated fibroblasts’-- more than meets the eye. Trends in Molecular Medicine 19, 447-453 Google Scholar
53. Calvo, F. et al. (2013) Mechanotransduction and YAP-dependent matrix remodelling is required for the generation and maintenance of cancer-associated fibroblasts. Nature Cell Biology 15, 637-646 Google Scholar
54. Shao, D.D. et al. (2014) KRAS and YAP1 converge to regulate EMT and tumor survival. Cell 158, 171-184 CrossRefGoogle ScholarPubMed
55. Kapoor, A. et al. (2014) Yap1 activation enables bypass of oncogenic Kras addiction in pancreatic cancer. Cell 158, 185-197 Google Scholar
56. Basu, S. et al. (2003) Akt phosphorylates the Yes-associated protein, YAP, to induce interaction with 14-3-3 and attenuation of p73-mediated apoptosis. Molecular Cell 11, 11-23 Google Scholar
57. Matallanas, D. et al. (2007) RASSF1A elicits apoptosis through an MST2 pathway directing proapoptotic transcription by the p73 tumor suppressor protein. Molecular Cell 27, 962-975 Google Scholar
58. Strano, S. et al. (2005) The transcriptional coactivator Yes-associated protein drives p73 gene-target specificity in response to DNA Damage. Molecular Cell 18, 447-459 Google Scholar
59. Yuan, M. et al. (2008) Yes-associated protein (YAP) functions as a tumor suppressor in breast. Cell Death & Differentiation 15, 1752-1759 Google Scholar
60. Danovi, S.A. et al. (2008) Yes-associated protein (YAP) is a critical mediator of c-Jun-dependent apoptosis. Cell Death & Differentiation 15, 217-219 Google Scholar
61. Levy, D. et al. (2007) The Yes-associated protein 1 stabilizes p73 by preventing Itch-mediated ubiquitination of p73. Cell Death & Differentiation 14, 743-751 Google Scholar
62. Strano, S. et al. (2001) Physical interaction with Yes-associated protein enhances p73 transcriptional activity. Journal of Biological Chemistry 276, 15164-15173 Google Scholar
63. Carter, S.L. et al. (1994) Loss of heterozygosity at 11q22-q23 in breast cancer. Cancer Research 54, 6270-6274 Google Scholar
64. Gudmundsson, J. et al. (1995) Loss of heterozygosity at chromosome 11 in breast cancer: association of prognostic factors with genetic alterations. British Journal of Cancer 72, 696-701 Google Scholar
65. Hampton, G.M. et al. (1994) Loss of heterozygosity in sporadic human breast carcinoma: a common region between 11q22 and 11q23.3. Cancer Research 54, 4586-4589 Google ScholarPubMed
66. Winqvist, R. et al. (1995) Loss of heterozygosity for chromosome 11 in primary human breast tumors is associated with poor survival after metastasis. Cancer Research 55, 2660-2664 Google Scholar
67. Yu, S.J. et al. (2013) MicroRNA-200a promotes anoikis resistance and metastasis by targeting YAP1 in human breast cancer. Clinical Cancer Research 19, 1389-1399 CrossRefGoogle ScholarPubMed
68. Bonnet, D. and Dick, J.E. (1997) Human acute myeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell. Nature Medicine 3, 730-737 CrossRefGoogle ScholarPubMed
69. Al-Hajj, M. et al. (2003) Prospective identification of tumorigenic breast cancer cells. Proceedings of the National Academy of Sciences of the United States of America 100, 3983-3988 CrossRefGoogle ScholarPubMed
70. Ricci-Vitiani, L. et al. (2007) Identification and expansion of human colon-cancer-initiating cells. Nature 445, 111-115 Google Scholar
71. Eramo, A. et al. (2008) Identification and expansion of the tumorigenic lung cancer stem cell population. Cell Death & Differentiation 15, 504-514 CrossRefGoogle ScholarPubMed
72. Singh, S.K. et al. (2004) Identification of human brain tumour initiating cells. Nature 432, 396-401 Google Scholar
73. Todaro, M. et al. (2010) Tumorigenic and metastatic activity of human thyroid cancer stem cells. Cancer Research 70, 8874-8885 Google Scholar
74. Prince, M.E. et al. (2007) Identification of a subpopulation of cells with cancer stem cell properties inhead and neck squamous cell carcinoma. Proceedings of the National Academy of Sciences of the United States of America 104, 973-978 Google Scholar
75. Li, C. et al. (2007) Identification of pancreatic cancer stem cells. Cancer Research 67, 1030-1037 Google Scholar
76. Collins, A.T. et al. (2005) Prospective identification of tumorigenic prostate cancer stem cells. Cancer Research 65, 10946-10951 Google Scholar
77. Gao, M.Q. et al. (2010) CD24+ cells from hierarchically organized ovarian cancer are enriched in cancer stem cells. Oncogene 29, 2672-2680 Google Scholar
78. Greaves, M. and Maley, C.C. (2012) Clonal evolution in cancer. Nature 481, 306-313 Google Scholar
79. Dieter, S.M. et al. (2011) Distinct types of tumor-initiating cells form human colon cancer tumors and metastases. Cell Stem Cell 9, 357-365 Google Scholar
80. Piccirillo, S.G. et al. (2009) Distinct pools of cancer stem-like cells coexist within human glioblastomas and display different tumorigenicity and independent genomic evolution. Oncogene 28, 1807-1811 CrossRefGoogle ScholarPubMed
81. Anderson, K. et al. (2011) Genetic variegation of clonal architecture and propagating cells in leukaemia. Nature 469, 356-361 Google Scholar
82. Notta, F. et al. (2011) Evolution of human BCR-ABL1 lymphoblastic leukaemia-initiating cells. Nature 469, 362-367 Google Scholar
83. Mani, S.A. et al. (2008) The epithelial–mesenchymal transition generates cells with properties of stem cells. Cell 133, 704-715 CrossRefGoogle ScholarPubMed
84. Li, Z. et al. (2009) Hypoxia-inducible factors regulate tumorigenic capacity of glioma stem cells. Cancer Cell 15, 501-513 Google Scholar
85. Hjelmeland, A.B. et al. (2011) Acidic stress promotes a glioma stem cell phenotype. Cell Death & Differentiation 18, 829-840 Google Scholar
86. Todaro, M. et al. (2014) CD44v6 is a marker of constitutive and reprogrammed cancer stem cells driving colon cancer metastasis. Cell Stem Cell 14, 342-356 CrossRefGoogle ScholarPubMed
87. Mo, J.S., Park, H.W. and Guan, K.L. (2014) The Hippo signaling pathway in stem cell biology and cancer. EMBO Reports 15, 642-656 Google Scholar
88. Cordenonsi, M. et al. (2011) The Hippo transducer TAZ confers cancer stem cell-related traits on breast cancer cells. Cell 147, 759-772 Google Scholar
89. Maugeri-Saccà, M., Zeuner, A. and De Maria, R. (2011) Therapeutic targeting of cancer stem cells. Frontiers in Oncology 1, 10 doi: 10.3389/fonc.2011.00010 Google Scholar
90. Lai, D., Ho, K.C., Hao, Y. and Yang, X. (2011) Taxol resistance in breast cancer cells is mediated by the hippo pathway component TAZ and its downstream transcriptional targets Cyr61 and CTGF. Cancer Research 71, 2728-2738 Google Scholar
91. Li, Y.W. et al. (2015) Characterization of TAZ domains important for the induction of breast cancer stem cell properties and tumorigenesis. Cell Cycle 14, 146-156 Google Scholar
92. Xiang, L. et al. (2014) Hypoxia-inducible factor 1 mediates TAZ expression and nuclear localization to induce the breast cancer stem cell phenotype. Oncotarget 5, 12509-12527 Google Scholar
93. Chang, C. et al. (2015) A laminin 511 matrix is regulated by TAZ and functions as the ligand for the α6Bβ1 integrin to sustain breast cancer stem cells. Genes & Development 29, 1-6 Google Scholar
94. Frangou, C. et al. (2014) Molecular profiling and computational network analysis of TAZ-mediated mammary tumorigenesis identifies actionable therapeutic targets. Oncotarget 5, 12166-12176 Google Scholar
95. Maugeri-Saccà, M., Vigneri, P. and De Maria, R. (2011) Cancer stem cells and chemosensitivity. Clinical Cancer Research 17, 4942-4947 Google Scholar
96. Maugeri-Saccà, M., Bartucci, M. and De Maria, R. (2012) DNA damage repair pathways in cancer stem cells. Molecular Cancer Therapeutics 11, 1627-1636 Google Scholar
97. Reis-Filho, J.S. and Pusztai, L. (2011) Gene expression profiling in breast cancer: classification, prognostication, and prediction. Lancet 378, 1812-1823 Google Scholar
98. Serrano, I. et al. (2013) Inactivation of the Hippo tumour suppressor pathway by integrin-linked kinase. Nature Communications 4, 2976 Google Scholar
99. Matteucci, E. et al. (2013) Bone metastatic process of breast cancer involves methylation state affecting E-cadherin expression through TAZ and WWOX nuclear effectors. European Journal of Cancer 49, 231-244 Google Scholar
100. Baselga, J. et al. (2012) Lapatinib with trastuzumab for HER2-positive early breast cancer (NeoALTTO): a randomised, open-label, multicentre, phase 3 trial. Lancet 379, 633-640 Google Scholar
101. Untch, M. et al. (2012) Lapatinib versus trastuzumab in combination with neoadjuvant anthracycline-taxane-based chemotherapy (GeparQuinto, GBG 44): a randomised phase 3 trial. The Lancet Oncology 13, 135-144 Google Scholar
102. Gianni, L. et al. (2012) Efficacy and safety of neoadjuvant pertuzumab and trastuzumab in women with locally advanced, inflammatory, or early HER2-positive breast cancer (NeoSphere): a randomised multicentre, open-label, phase 2 trial. The Lancet Oncology 13, 25-32 Google Scholar
103. Fumagalli, D. (2012) BIG-NABCG collaboration. A common language in neoadjuvant breast cancer clinical trials: proposals for standard definitions and endpoints. The Lancet Oncology 13, e240-248CrossRefGoogle Scholar
104. Liu-Chittenden, Y. et al. (2012) Genetic and pharmacological disruption of the TEAD-YAP complex suppresses the oncogenic activity of YAP. Genes & Development 26, 1300-1305 Google Scholar
105. Yu, F.X. et al. (2014) Mutant Gq/11 promote uveal melanoma tumorigenesis by activating YAP. Cancer Cell 25, 822-830 Google Scholar
106. Bao, Y. et al. (2011) A cell-based assay to screen stimulators of the Hippo pathway reveals the inhibitory effect of dobutamine on the YAP-dependent gene transcription. The Journal of Biochemistry 150, 199-208 Google Scholar
107. Rosenbluh, J. et al. (2012) β-Catenin-driven cancers require a YAP1 transcriptional complex for survival and tumorigenesis. Cell 151, 1457-1473 Google Scholar
108. Wang, Z. et al. (2014) Interplay of mevalonate and Hippo pathways regulates RHAMM transcription via YAP to modulate breast cancer cell motility. Proceedings of the National Academy of Sciences of the United States of America 111, E89-E98 Google Scholar