Nuclear beta-catenin expression and Wnt signalling: in defence of the dogma

Riccardo Fodde, I Tomlinson

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

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-beta-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 p-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 p-catenin in both the presence and, more often, the absence of KRAS mutations. Copyright (C) 2010 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Original languageUndefined/Unknown
Pages (from-to)239-241
Number of pages3
JournalJournal of Pathology
Volume221
Issue number3
Publication statusPublished - 2010

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