Please use this identifier to cite or link to this item: https://doi.org/10.1080/00313020410001671957
Title: The significance of the Wnt pathway in the pathology of human cancers
Authors: Karim, R.Z.
Tse, G.M.K.
Putti, T.C. 
Scolyer, R.A.
Lee, C.S.
Keywords: β-catenin
APC
Axin
Cancer
Frizzled membrane receptor
Fz
Neoplasm
Wingless-type protein
Wnt
Issue Date: Apr-2004
Citation: Karim, R.Z., Tse, G.M.K., Putti, T.C., Scolyer, R.A., Lee, C.S. (2004-04). The significance of the Wnt pathway in the pathology of human cancers. Pathology 36 (2) : 120-128. ScholarBank@NUS Repository. https://doi.org/10.1080/00313020410001671957
Abstract: The wingless-type (Wnt) signalling transduction pathway is essentially a network of a number of separate but interacting pathways. Specific Wnt ligands bind to their target 'frizzled' membrane receptor and interfere with the multi-protein destruction complex, resulting in downstream activation of gene transcription by β-catenin. Simplistically, the multi-protein destruction complex involves Axin and APC serving as scaffolds binding both β-catenin and GSK3, to facilitate phosphorylation of β-catenin by GSK-3β. Phosphorylated β-catenin is degraded in proteasomes by the ubiquination machinery. Unphosphorylated β-catenin accumulates and associates with nuclear transcription factors leading to the eventual transcription and expression of target genes such as c-myc, c-jun, Fra and cyclin D1. There are several regulatory mechanisms for the down-regulation of the Wnt/ β-catenin signal, perhaps reflecting the pivotal nature of the pathway and the detrimental consequences of inappropriate activation. There has been intense investigation into the role of Wnt genes in human cancer. Although no documentation is made of any mutation or amplification of genes encoding Wnt ligands or receptors linked to human cancer to date, several components of the Wnt pathway have been implicated in carcinogenesis, especially APC and β-catenin.
Source Title: Pathology
URI: http://scholarbank.nus.edu.sg/handle/10635/130524
ISSN: 00313025
DOI: 10.1080/00313020410001671957
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