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@ARTICLE{Whitehead:2105,
      author       = {Whitehead, J. and Vignjevic, D. and Fütterer, C. and
                      Beaurepaire, E. and Robine, S. and Farge, E.},
      title        = {{M}echanical factors activate ß-catenin-dependent oncogene
                      expression in {APC}1638{N}/+ mouse colon},
      journal      = {HFSP journal},
      volume       = {2},
      issn         = {1955-205X},
      address      = {HFSP Publishing},
      publisher    = {HFSP Publishing, PubMed Central},
      reportid     = {PreJuSER-2105},
      pages        = {286 - 294},
      year         = {2008},
      note         = {JW was supported by a French Ministry of Education $\&$
                      Research fellowship and a Marie Curie Intra-European
                      fellowship. This work was supported by grants from ARC
                      (3536), INSERM (ITS2005), HSFP (RGP0014/2006-C) and Equipe
                      Labellisee La Ligue (EL2008. LNCC/SR1). JW carried out the
                      experimental work and imaging, and prepared the manuscript;
                      DJ aided in tissue preparation; CF designed the apparatus;
                      SR provided mice; EB carried out the 2PEF microscopy; EF
                      initiated the project. JW $\&$ EF analyzed the data, and all
                      authors contributed to project planning and manuscript
                      preparation. Thanks to Francois Waharte (Cell and Tissue
                      Imaging Facility, UMR144 CNRS/Institut Curie) for confocal
                      imaging assistance, to Jacques Prost and Padra Ahmadi
                      (UMR168 CNRS/Institut Curie) for experimental advice, and to
                      Olivier Delattre, Xavier Sastre, Daniel Louvard, and members
                      of the Robine lab for helpful discussions.},
      abstract     = {beta-catenin acts as a critical regulator of
                      gastrointestinal homeostasis through its control of the Wnt
                      signaling pathway, and genetic or epigenetic lesions which
                      activate Wnt signaling are the primary feature of colon
                      cancer. beta-catenin is also a key element of
                      mechanotranscription pathways, leading to upregulation of
                      master developmental gene expression during Drosophila
                      gastrulation, or regulating mammalian bone development and
                      maintenance. Here we investigate the impact of mechanical
                      stimulation on the initiation of colon cancer. Myc and
                      Twist1, two oncogenes regulated through beta-catenin, are
                      expressed in response to transient compression in APC
                      deficient (APC(1638N+)) colon tissue explants, but not in
                      wild-type colon explants. Mechanical stimulation of
                      APC(1638N+) tissue leads to the phosphorylation of
                      beta-catenin at tyrosine 654, the site of interaction with
                      E-cadherin, as well as to increased nuclear localization of
                      beta-catenin. The mechanical activation of Myc and Twist1
                      expression in APC(1638N+) colon can be prevented by blocking
                      beta-catenin phosphorylation using Src kinase inhibitors.
                      Microenvironmental signals are known to cooperate with
                      genetic lesions to promote the nuclear beta-catenin
                      accumulation which drives colon cancer. Here we demonstrate
                      that when APC is limiting, mechanical strain, such as that
                      associated with intestinal transit or tumor growth, can be
                      interpreted by cells of preneoplastic colon tissue as a
                      signal to initiate a beta-catenin dependent transcriptional
                      program characteristic of cancer.},
      keywords     = {J (WoSType)},
      cin          = {INB-1},
      ddc          = {610},
      cid          = {I:(DE-Juel1)VDB804},
      pnm          = {Funktion und Dysfunktion des Nervensystems},
      pid          = {G:(DE-Juel1)FUEK409},
      shelfmark    = {Multidisciplinary Sciences},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:19404440},
      pmc          = {pmc:PMC2639941},
      UT           = {WOS:000259736700008},
      doi          = {10.2976/1.2955566},
      url          = {https://juser.fz-juelich.de/record/2105},
}