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. 2019 Jul 7;25(25):3151–3167. doi: 10.3748/wjg.v25.i25.3151

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©The Author(s) 2019. Published by Baishideng Publishing Group Inc. All rights reserved.

This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.

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Aberrant activation of the Wnt/β-catenin signaling pathway in hepatocellular carcinoma. A: Wnt signaling is inactive in the absence of Wnt ligands (OFF); B: Wnt signaling can be activated by various molecules in HCC (ON). HBV and HCV can active Wnt/β-catenin signaling by activating TCF or inhibiting GSK3β; HBx can silence SFRPs to activate Wnt signaling; LncTCF7 triggers Wnt7a and TCF7 expression to activate Wnt signaling. Lines ending with arrows or bars indicate activating or inhibitory effects, respectively. HIF1α: Hypoxia-inducible factor 1α; LEF: Lymphoid enhancer-binding factor; LRP: Low-density lipoprotein receptor-related protein; TCF: T cell factor; FZD: Frizzled; E-cad: E-cadherin; SFRPs: Secreted frizzled-related proteins; CTGF: Connective tissue growth factor; WISP2: Wnt1 inducible signaling pathway protein 2.