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Comment
. 2015 May;236(1):1-4.
doi: 10.1002/path.4512. Epub 2015 Mar 3.

CUL4B: a novel epigenetic driver in Wnt/β-catenin-dependent hepatocarcinogenesis

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Comment

CUL4B: a novel epigenetic driver in Wnt/β-catenin-dependent hepatocarcinogenesis

Myth T S Mok et al. J Pathol. 2015 May.

Abstract

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.

Keywords: CUL4B; EZH2; Wnt antagonists; hepatocellular carcinoma; ubiquitination; β-catenin.

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