CUL4B: a novel epigenetic driver in Wnt/β-catenin-dependent hepatocarcinogenesis
- PMID: 25664533
- DOI: 10.1002/path.4512
CUL4B: a novel epigenetic driver in Wnt/β-catenin-dependent hepatocarcinogenesis
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.
Copyright © 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Comment on
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CUL4B activates Wnt/β-catenin signalling in hepatocellular carcinoma by repressing Wnt antagonists.J Pathol. 2015 Apr;235(5):784-95. doi: 10.1002/path.4492. Epub 2015 Jan 23. J Pathol. 2015. PMID: 25430888
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