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Int. J. Mol. Sci. 2018, 19(1), 313; doi:10.3390/ijms19010313

Deregulation of Frizzled Receptors in Hepatocellular Carcinoma

Department of Pathology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China
State Key Laboratory for Liver Research, The University of Hong Kong, Hong Kong, China
Author to whom correspondence should be addressed.
Received: 22 December 2017 / Revised: 14 January 2018 / Accepted: 19 January 2018 / Published: 21 January 2018
(This article belongs to the Special Issue Cancer-Driver G Protein-Coupled Receptors as Therapeutic Targets)
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G protein-coupled receptors (GPCRs) have a substantial role in tumorigenesis and are described as a “cancer driver”. Aberrant expression or activation of GPCRs leads to the deregulation of downstream signaling pathways, thereby promoting cancer progression. In hepatocellular carcinoma (HCC), the Wnt signaling pathway is frequently activated and it is associated with an aggressive HCC phenotype. Frizzled (FZD) receptors, a family member of GPCRs, are known to mediate Wnt signaling. Accumulating findings have revealed the deregulation of FZD receptors in HCC and their functional roles have been implicated in HCC progression. Given the important role of FZD receptors in HCC, we summarize here the expression pattern of FZD receptors in HCC and their corresponding functional roles during HCC progression. We also further review and highlight the potential targeting of FZD receptors as an alternative therapeutic strategy in HCC. View Full-Text
Keywords: hepatocellular carcinoma; G protein-coupled receptors; Frizzled receptors; Wnt signaling hepatocellular carcinoma; G protein-coupled receptors; Frizzled receptors; Wnt signaling

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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Chan, K.K.-S.; Lo, R.C.-L. Deregulation of Frizzled Receptors in Hepatocellular Carcinoma. Int. J. Mol. Sci. 2018, 19, 313.

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