32
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      WNT signalling in prostate cancer

      ,
      Nature Reviews Urology
      Springer Nature

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          WNT signalling pathway components are potentially important in prostate tumours, particularly in the development of castration-resistant prostate cancer and in the prostate tumour microenvironment. Here, Murillo-Garzón and Kypta describe our current understanding of WNT signalling in prostate cancer and discuss the potential of drugs that target this pathway.

          Related collections

          Most cited references115

          • Record: found
          • Abstract: not found
          • Article: not found

          AP-1: a double-edged sword in tumorigenesis.

            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Wnt signalling and its impact on development and cancer.

            The Wnt signalling pathway is an ancient system that has been highly conserved during evolution. It has a crucial role in the embryonic development of all animal species, in the regeneration of tissues in adult organisms and in many other processes. Mutations or deregulated expression of components of the Wnt pathway can induce disease, most importantly cancer. The first gene to be identified that encodes a Wnt signalling component, Int1 (integration 1), was molecularly characterized from mouse tumour cells 25 years ago. In parallel, the homologous gene Wingless in Drosophila melanogaster, which produces developmental defects in embryos, was characterized. Since then, further components of the Wnt pathway have been identified and their epistatic relationships have been defined. This article is a Timeline of crucial discoveries about the components and functions of this essential pathway.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              YAP/TAZ incorporation in the β-catenin destruction complex orchestrates the Wnt response.

              The Hippo transducers YAP/TAZ have been shown to play positive, as well as negative, roles in Wnt signaling, but the underlying mechanisms remain unclear. Here, we provide biochemical, functional, and genetic evidence that YAP and TAZ are integral components of the β-catenin destruction complex that serves as cytoplasmic sink for YAP/TAZ. In Wnt-ON cells, YAP/TAZ are physically dislodged from the destruction complex, allowing their nuclear accumulation and activation of Wnt/YAP/TAZ-dependent biological effects. YAP/TAZ are required for intestinal crypt overgrowth induced by APC deficiency and for crypt regeneration ex vivo. In Wnt-OFF cells, YAP/TAZ are essential for β-TrCP recruitment to the complex and β-catenin inactivation. In Wnt-ON cells, release of YAP/TAZ from the complex is instrumental for Wnt/β-catenin signaling. In line, the β-catenin-dependent maintenance of ES cells in an undifferentiated state is sustained by loss of YAP/TAZ. This work reveals an unprecedented signaling framework relevant for organ size control, regeneration, and tumor suppression. Copyright © 2014 Elsevier Inc. All rights reserved.
                Bookmark

                Author and article information

                Journal
                Nature Reviews Urology
                Nat Rev Urol
                Springer Nature
                1759-4812
                1759-4820
                September 12 2017
                September 12 2017
                :
                :
                Article
                10.1038/nrurol.2017.144
                28895566
                664eedc5-a45e-42a2-97e4-fed0cb8becb3
                © 2017
                History

                Comments

                Comment on this article