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Non-canonical WNT/PCP signalling in cancer: Fzd6 takes centre stage

Frizzled receptors are the mediators of the wnt canonical and non-canonical pathways, which play fundamental roles in cell differentiation and organism development. A large body of work indicates that dysregulation of wnt signalling is a feature of oncogenic transformation, but most of the studies p...

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Detalles Bibliográficos
Autores principales: Corda, G, Sala, A
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5541719/
https://www.ncbi.nlm.nih.gov/pubmed/28737757
http://dx.doi.org/10.1038/oncsis.2017.69
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author Corda, G
Sala, A
author_facet Corda, G
Sala, A
author_sort Corda, G
collection PubMed
description Frizzled receptors are the mediators of the wnt canonical and non-canonical pathways, which play fundamental roles in cell differentiation and organism development. A large body of work indicates that dysregulation of wnt signalling is a feature of oncogenic transformation, but most of the studies published so far focus on the assessment of the consequences of aberrations of the canonical pathway in human cancer. In this review, we discuss the emerging role of the wnt non-canonical pathway regulated by frizzled receptor 6 (Fzd6) in the pathogenesis of different types of human malignancies. The function played by Fzd6 in the physiology of normal and cancer cells has been highlighted in the view that an increased knowledge of the signalling pathways upstream and downstream of this receptor could ultimately result in the identification of new targets for cancer therapy.
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spelling pubmed-55417192017-08-08 Non-canonical WNT/PCP signalling in cancer: Fzd6 takes centre stage Corda, G Sala, A Oncogenesis Review Frizzled receptors are the mediators of the wnt canonical and non-canonical pathways, which play fundamental roles in cell differentiation and organism development. A large body of work indicates that dysregulation of wnt signalling is a feature of oncogenic transformation, but most of the studies published so far focus on the assessment of the consequences of aberrations of the canonical pathway in human cancer. In this review, we discuss the emerging role of the wnt non-canonical pathway regulated by frizzled receptor 6 (Fzd6) in the pathogenesis of different types of human malignancies. The function played by Fzd6 in the physiology of normal and cancer cells has been highlighted in the view that an increased knowledge of the signalling pathways upstream and downstream of this receptor could ultimately result in the identification of new targets for cancer therapy. Nature Publishing Group 2017-07 2017-07-24 /pmc/articles/PMC5541719/ /pubmed/28737757 http://dx.doi.org/10.1038/oncsis.2017.69 Text en Copyright © 2017 The Author(s) http://creativecommons.org/licenses/by/4.0/ Oncogenesis is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Review
Corda, G
Sala, A
Non-canonical WNT/PCP signalling in cancer: Fzd6 takes centre stage
title Non-canonical WNT/PCP signalling in cancer: Fzd6 takes centre stage
title_full Non-canonical WNT/PCP signalling in cancer: Fzd6 takes centre stage
title_fullStr Non-canonical WNT/PCP signalling in cancer: Fzd6 takes centre stage
title_full_unstemmed Non-canonical WNT/PCP signalling in cancer: Fzd6 takes centre stage
title_short Non-canonical WNT/PCP signalling in cancer: Fzd6 takes centre stage
title_sort non-canonical wnt/pcp signalling in cancer: fzd6 takes centre stage
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5541719/
https://www.ncbi.nlm.nih.gov/pubmed/28737757
http://dx.doi.org/10.1038/oncsis.2017.69
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