Wnt signalling in mammalian development and cancer

Smalley, Matthew John ORCID: https://orcid.org/0000-0001-9540-1146 and Dale, Trevor Clive ORCID: https://orcid.org/0000-0002-4880-9963 1999. Wnt signalling in mammalian development and cancer. Cancer and Metastasis Reviews 18 (2) , pp. 215-230. 10.1023/A:1006369223282

Full text not available from this repository.

Abstract

Wnt signalling is involved in a variety of mammalian developmental processes, including cell proliferation, differentiation and epithelial-mesenchymal interactions, through which they contribute to the development of tissues and organs such as the limbs, the brain, the reproductive tract and the kidney. Wnts are secreted ligands that control cell processes via at least two pathways, one of which, the 'canonical' Wnt signalling pathway, operates through the cytosolic stabilisation of a transcriptional co-factor, beta-catenin. This is achieved by downregulating the activity of a beta-catenin turnover complex. Evidence from tumour expression studies, transgenic animals and in vitro experiments suggests that inappropriate activation of the canonical Wnt signalling pathway is a major feature in human neoplasia and that oncogenic activation of this pathway can occur at many levels. Inappropriate expression of the Wnt ligand and Wnt binding proteins have been found in a variety of human tumours. Further downstream, dysregulation of the beta-catenin turnover complex, by loss of the Adenomatous Polyposis Coli or Protein Phosphatase 2A proteins, or by activating mutations of beta-catenin, has been found in several tumour types, and is believed to be a key step in neoplastic progression. Transcriptional targets of the Wnt pathway include the cellular oncogenes cyclin D1 and c-myc. Activation of the Wnt signalling pathway by various means can therefore be a primary cause in oncogenesis, affecting cell proliferation, morphology and contact inhibition, as well as co-operating with other oncogenes in multistep tumour progression.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Biosciences European Cancer Stem Cell Research Institute (ECSCRI)
Publisher:	Springer
ISSN:	0167-7659
Last Modified:	27 Oct 2022 09:09
URI:	https://orca.cardiff.ac.uk/id/eprint/64564

Citation Data

Cited 187 times in Scopus. View in Scopus. Powered By Scopus® Data

Actions (repository staff only)

Edit Item