[an error occurred while processing this directive]

Crosstalk of Hippo/YAP and Wnt/β-catenin pathways

Expand
  • 1. Key Laboratory of Molecular Medicine, Ministry of Education, Shanghai Medical College, Fudan University, Shanghai 200032, China; 
    2. Institutes of Biomedical Sciences, Research Center for Birth Defects, Fudan University, Shanghai 200032, China

Received date: 2013-08-26

  Revised date: 2013-11-25

  Online published: 2014-01-25

Abstract

Wnt/β-catenin and Hippo/YAP pathways are known to be important for development, growth, organogenesis, and maintenance of adult stem cells. In mammalian cells, Wnt signalling stabilises cytoplasmic β-catenin through several core molecules to promote β-catenin to enter the nucleus, thus delivers the growth -promoting signal. Hippo kinase cascade pathway promotes cytoplasmic localization of YAP/TAZ, which restricts cell proliferation and induces apoptosis. Deregula-tion of these two pathways could lead to tumorigenesis. Growing data indicate that these two pathways influence each other in a number of ways to properly regulate tissue growth and repair. Elucidating the regulatory mechanism and biological functions of Hippo/YAP and Wnt/β-catenin pathways might reveal potential targets for tumor therapeutic intervention. In this review, we discuss on the interactions between Wnt/β-catenin and Hippo/YAP pathways, and how these interactions contribute to tumorigenesis.

Cite this article

Fei Xu, Jin Zhang, Duan Ma . Crosstalk of Hippo/YAP and Wnt/β-catenin pathways[J]. Hereditas(Beijing), 2014 , 36(2) : 95 -102 . DOI: 10.3724/SP.J.1005.2014.0095

References

[1] Anastas JN, Moon RT. WNT signalling pathways as therapeutic targets in cancer. Nat Rev Cancer, 2013, 13(1): 11–26. <\p>

[2] Hoffmeyer K, Raggioli A, Rudloff S, Anton R, Hierholzer A, Del Valle I, Hein K, Vogt R, Kemler R. Wnt/β-catenin signaling regulates telomerase in stem cells and cancer cells. Science, 2012, 336(6088): 1549–1554. <\p>

[3] Ouyang H, Zhuo YH, Zhang K. WNT signaling in stem cell differentiation and tumor formation. J Clin Invest, 2013, 123(4): 1422–1424. <\p>

[4] Watson AL, Rahrmann EP, Moriarity BS, Choi K, Conboy CB, Greeley AD, Halfond AL, Anderson LK, Wahl BR, Keng VW, Rizzardi AE, Forster CL, Collins MH, Sarver A, Wallace MR, Schmechel SC, Ratner N, Largaespada DA. Canonical Wnt/β-catenin signaling drives human schwann cell transformation, progression, and tumor maintenance. Cancer Discov, 2013, 3(6): 674–689. <\p>

[5] Yu FX, Guan KL. The Hippo pathway: regulators and regulations. Genes Dev, 2013, 27(4): 355–371. <\p>

[6] Huang J, Wu S, Barrera J, Matthews K, Pan DJ. The Hippo signaling pathway coordinately regulates cell pro-liferation and apoptosis by inactivating Yorkie, the Dro-sophila Homolog of YAP. Cell, 2005, 122(3): 421–434. <\p>

[7] Goulev Y, Fauny JD, Gonzalez-Marti B, Flagiello D, Sil-ber J, Zider A. SCALLOPED interacts with YORKIE, the nuclear effector of the hippo tumor-suppressor pathway in Drosophila. Curr Biol, 2008, 18(6): 435–441. <\p>

[8] Kaneko KJ, DePamphilis ML. Regulation of gene expres-sion at the beginning of mammalian development and the TEAD family of transcription factors. Dev Genet, 1998, 22(1): 43–55. <\p>

[9] Sharma RP, Chopra VL. Effect of the Wingless (wg1) mu-tation on wing and haltere development in Drosophila melanogaster. Dev Biol, 1976, 48(2): 461–465. <\p>

[10] Nusse R, Varmus HE. Many tumors induced by the mouse mammary tumor virus contain a provirus integrated in the same region of the host genome. Cell, 1982, 31(1): 99– 109. <\p>

[11] Cabrera CV, Alonso MC, Johnston P, Phillips RG, Law-rence PA. Phenocopies induced with antisense RNA iden-tify the wingless gene. Cell, 1987, 50(4): 659–663. <\p>

[12] Rijsewijk F, Schuermann M, Wagenaar E, Parren P, Weigel D, Nusse R. The Drosophila homolog of the mouse mammary oncogene int-1 is identical to the segment po-larity gene wingless. Cell, 1987, 50(4): 649–657. <\p>

[13] Willert K, Brown JD, Danenberg E, Duncan AW, Weiss-man IL, Reya T, Yates JR, Nusse R. Wnt proteins are lipid-modified and can act as stem cell growth factors. Nature, 2003, 423(6938): 448–452. <\p>

[14] Hsieh JC, Rattner A, Smallwood PM, Nathans J. Bio-chemical characterization of Wnt-frizzled interactions us-ing a soluble, biologically active vertebrate Wnt protein. Proc Natl Acad Sci USA, 1999, 96(7): 3546–3551. <\p>

[15] Dann CE, Hsieh JC, Rattner A, Sharma D, Nathans J, Leahy DJ. Insights into Wnt binding and signalling from the structures of two Frizzled cysteine-rich domains. Na-ture, 2001, 412(6842): 86–90. <\p>

[16] Kimelman D, Xu W. beta-catenin destruction complex: in-sights and questions from a structural perspective. Onco-gene, 2006, 25(57): 7482–7491. <\p>

[17] Maher MT, Mo R, Flozak AS, Peled ON, Gottardi CJ. Beta-catenin phosphorylated at serine 45 is spatially un-coupled from beta-catenin phosphorylated in the GSK3 domain: implications for signaling. PloS ONE, 2010, 5(4): e10184. <\p>

[18] Aberle H, Bauer A, Stappert J, Kispert A, Kemler R. beta-catenin is a target for the ubiquitin-proteasome path-way. EMBO J, 1997, 16(13): 3797–3804. <\p>

[19] Marikawa Y, Elinson RP. beta-TrCP is a negative regulator of the Wnt/beta-catenin signaling pathway and dorsal axis formation in X

Outlines

/