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  • Open Access

    CORRECTION

    TRAF4 Regulates Migration, Invasion, and Epithelial–Mesenchymal Transition via PI3K/AKT Signaling in Hepatocellular Carcinoma

    Kairui Liu*, Xiaolin Wu*, Xian Zang, Zejian Huang*, Zeyu Lin, Wenliang Tan*, Xiang Wu*, Wenrou Hu*, Baoqi Li*, Lei Zhang*

    Oncology Research, Vol.28, No.5, pp. 559-560, 2020, DOI:10.3727/096504020X16032056440102

    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 More >

  • Open Access

    ARTICLE

    TRAF4 Regulates Migration, Invasion, and Epithelial–Mesenchymal Transition via PI3K/AKT Signaling in Hepatocellular Carcinoma

    Kairui Liu*, Xiaolin Wu*, Xian Zang, Zejian Huang*, Zeyu Lin, Wenliang Tan*, Xiang Wu*, Wenrou Hu*, Baoqi Li*, Lei Zhang*

    Oncology Research, Vol.25, No.8, pp. 1329-1340, 2017, DOI:10.3727/096504017X14876227286564

    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 More >

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