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. 2017 Jul 20;14(3):3291–3296. doi: 10.3892/ol.2017.6622

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Copyright: © Shan et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 2. — YAP is regulated by various factors during hepatocarcinogenesis in addition to the members of the Hippo signaling pathway. These factors have an important role in YAP-associated hepatocellular carcinoma. BTRC and TRIB2 inhibit the overexpression of YAP. The interactions between YAP and other factors (CREB, c-Myc, CD166 and MCAM) promote hepatocarcinogenesis. High/hippo dependent refers to the effects of BTRC on YAP, which are dependent on the Hippo pathway. When BTRC is overexpressed, or the Hippo pathway is activated and YAP turnover is inhibited; however, at normal levels of BTRC, YAP is protected from degradation. BTRC, β-transducin repeat-containing E3 ubiquitin protein ligase; CD, cluster of differentiation; CREB, cyclic adenosine monophosphate response element-binding protein; C/EBPα, CCAAT/enhancer binding protein α; MAPK14, mitogen-activated protein kinase 14; MCAM, melanoma cell adhesion molecule; p-MEK1, phosphorylated-mitogen-activated protein kinase; TRIB2, tribbles homolog 2; YAP, yes-associated protein.