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CUL4B : a novel epigenetic driver in Wnt/β‐catenin‐dependent hepatocarcinogenesis
Author(s) -
Mok Myth T.S.,
Cheng Alfred S.L.
Publication year - 2015
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.4512
Subject(s) - wnt signaling pathway , ubiquitin ligase , ubiquitin , cancer research , ezh2 , epigenetics , catenin , biology , hepatocellular carcinoma , cullin , microbiology and biotechnology , signal transduction , genetics , gene
Emerging evidence indicates that Cullin 4B ( CUL4B ), a major component of ubiquitin ligase complexes, is over‐expressed in diverse cancer types with pro‐tumourigenic effects. In this issue of the Journal of Pathology , Yuan and colleagues [6] elucidated the oncogenic activity of CUL4B in hepatocellular carcinoma ( HCC ) and delineated its role in driving Wnt/β‐catenin signalling. In addition to the stabilization of β‐catenin protein against proteasomal degradation, CUL4B also acts in concert with enhancer of Zeste homologue 2 ( EZH2 ) to concordantly silence multiple Wnt inhibitors. These findings provide significant mechanistic insights into the epigenetic activation of the Wnt/β‐catenin pathway in HCC and shed light on the functional importance of ubiquitination in this intricate regulatory system. Copyright © 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.