@Article{096504017X14876227286564,
AUTHOR = {Kairui Liu, Xiaolin Wu, Xian Zang, Zejian Huang, Zeyu Lin, Wenliang Tan, Xiang Wu, Wenrou Hu, Baoqi Li, Lei Zhang},
TITLE = {TRAF4 Regulates Migration, Invasion, and Epithelial–Mesenchymal  Transition via PI3K/AKT Signaling in Hepatocellular Carcinoma},
JOURNAL = {Oncology Research},
VOLUME = {25},
YEAR = {2017},
NUMBER = {8},
PAGES = {1329--1340},
URL = {http://www.techscience.com/or/v25n8/56917},
ISSN = {1555-3906},
ABSTRACT = {Overexpression of the tumor necrosis factor receptor-associated factor 4 (TRAF4) has been detected in many 
cancer types and is considered to foster tumor progression. However, the role of TRAF4 in hepatocellular carcinoma (HCC) remains elusive. In this study, we found that TRAF4 was highly expressed in HCC cell lines and 
HCC tissues compared with normal liver cell lines and adjacent noncancerous tissues. TRAF4 overexpression 
in HCC tissues was correlated with tumor quantity and vascular invasion. In vitro studies showed that TRAF4 
was associated with HCC cell migration and invasion. An in vivo study verified that TRAF4 overexpression facilitated metastasis in nude mice. In addition, overexpressed TRAF4 promoted the phosphorylation of 
Akt and induced Slug overexpression, leading to downregulated E-cadherin and upregulated vimentin, while 
silencing TRAF4 moderated the phosphorylation of Akt and repressed the expression of Slug, which resulted 
in upregulated E-cadherin and downregulated vimentin. These effects were inversed after pretreatment of the 
PI3K/Akt inhibitor LY294002 or overexpression of constitutively active Akt1. Our study demonstrated that 
TRAF4 was involved in promoting HCC cell migration and invasion. The process was induced by the EMT 
through activation of the PI3K/Akt signaling pathway.},
DOI = {10.3727/096504017X14876227286564}
}