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Nuclear β‐catenin expression and Wnt signalling: in defence of the dogma
Author(s) -
Fodde Riccardo,
Tomlinson Ian
Publication year - 2010
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.2718
Subject(s) - wnt signaling pathway , kras , biology , catenin , cancer research , microbiology and biotechnology , repressor , beta catenin , suppressor , mutation , genetics , signal transduction , gene , gene expression
Inactivation of the APC tumour suppressor gene represents the rate‐limiting event in colorectal cancer. Loss of APC function leads to constitutive activation of the canonical Wnt–β‐catenin signalling pathway, thus resulting into a broad spectrum of cellular defects, ranging from stem cell self‐renewal and differentiation, apoptosis, migration and proliferation. Recently, Phelps et al 1 presented an alternative model where loss of APC does not primarily result in Wnt signalling activation but rather involves the transcriptional co‐repressor CtBP1. According to this alternative scenario, oncogenic KRAS activation represents a conditio sine qua non for nuclear β‐catenin translocation and Wnt activation. In a recent issue of the Journal of Pathology , Obrador‐Hevia and collaborators 2 reaffirmed the broadly accepted textbook model by showing the presence of nuclear β‐catenin in both the presence and, more often, the absence of KRAS mutations. Copyright © 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.