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Polycomb group protein EZH2-mediated E-cadherin repression promotes metastasis of oral tongue squamous cell carcinoma

Authors

  • Cheng Wang,

    1. Center for Molecular Biology of Oral Diseases, College of Dentistry, University of Illinois at Chicago, Chicago, Illinois
    2. Department of Oral and Maxillofacial Surgery, Guanghua School and Research Institute of Stomatology, Sun Yat-Sen University, Guangzhou, Guangdong, China
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  • Xiqiang Liu,

    1. Center for Molecular Biology of Oral Diseases, College of Dentistry, University of Illinois at Chicago, Chicago, Illinois
    2. Department of Oral and Maxillofacial Surgery, Guanghua School and Research Institute of Stomatology, Sun Yat-Sen University, Guangzhou, Guangdong, China
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  • Zujian Chen,

    1. Center for Molecular Biology of Oral Diseases, College of Dentistry, University of Illinois at Chicago, Chicago, Illinois
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  • Hongzhang Huang,

    Corresponding author
    1. Department of Oral and Maxillofacial Surgery, Guanghua School and Research Institute of Stomatology, Sun Yat-Sen University, Guangzhou, Guangdong, China
    • Department of Oral and Maxillofacial Surgery, Guanghua School and Research Institute of Stomatology, Sun Yat-Sen University, Guangzhou 510055, China.
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  • Yi Jin,

    1. Center for Molecular Biology of Oral Diseases, College of Dentistry, University of Illinois at Chicago, Chicago, Illinois
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  • Antonia Kolokythas,

    1. Center for Molecular Biology of Oral Diseases, College of Dentistry, University of Illinois at Chicago, Chicago, Illinois
    2. Department of Oral and Maxillofacial Surgery, College of Dentistry, University of Illinois at Chicago, Chicago, Illinois
    3. Graduate College, UIC Cancer Center, University of Illinois at Chicago, Chicago, Illinois
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  • Anxun Wang,

    1. Center for Molecular Biology of Oral Diseases, College of Dentistry, University of Illinois at Chicago, Chicago, Illinois
    2. Department of Oral and Maxillofacial Surgery, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China
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  • Yang Dai,

    1. Graduate College, UIC Cancer Center, University of Illinois at Chicago, Chicago, Illinois
    2. Bioinformatics Program, Department of Bioengineering, College of Engineering, University of Illinois at Chicago, Chicago, Illinios
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  • David T.W. Wong,

    1. Dental Research Institute, School of Dentistry, Jonsson Comprehensive Cancer Center, University of California at Los Angeles, Los Angeles, California
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  • Xiaofeng Zhou

    Corresponding author
    1. Center for Molecular Biology of Oral Diseases, College of Dentistry, University of Illinois at Chicago, Chicago, Illinois
    2. Graduate College, UIC Cancer Center, University of Illinois at Chicago, Chicago, Illinois
    3. Department of Periodontics, College of Dentistry, University of Illinois at Chicago, Chicago, Illinois
    • Center for Molecular Biology of Oral Diseases, College of Dentistry, University of Illinois at Chicago, Chicago, IL 60612, USA.
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  • Conflict of interest: None declared.

  • Cheng Wang and Xiqiang Liu are contributed equally to this study.

Abstract

Enhancer of Zeste homolog 2 (EZH2) is a critical component of the polycomb-repressive complex 2 (PRC2) that regulates many essential biological processes, including embryogenesis and many developmental events. The oncogenic role of EZH2 has recently been implicated in several cancer types. In this study, we first confirmed that the over-expression of EZH2 is a frequent event in oral tongue squamous cell carcinoma (OTSCC). We further demonstrated that EZH2 over-expression is correlated with advanced stages of the disease and is associated with lymph node metastasis. Statistical analysis revealed that EZH2 over-expression was correlated with reduced overall survival. Furthermore, over-expression of EZH2 was correlated with reduced expression of tumor suppressor gene E-cadherin. These observations were confirmed in vitro, in which knockdown of EZH2-induced E-cadherin expression and reduced cell migration and invasion. In contrast, ectopic transfection of EZH2 led to reduced E-cadherin expression and enhanced cell migration and invasion. Furthermore, EZH2 may act on cell migration in part by suppressing the E-cadherin expression. Taken together, these data suggest that EZH2 plays major roles in the progression of OTSCC, and may serve as a biomarker or therapeutic target for patients at risk of metastasis. © 2011 Wiley Periodicals, Inc.

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