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Proteomic features of potential tumor suppressor NESG1 in nasopharyngeal carcinoma

Authors

  • Zhen Liu,

    1. Department of Pathology, Basic School of Guangzhou Medical College, Guangzhou, China
    2. Cancer Research Institute of Basic Medical School, Southern Medical University, Guangzhou, China
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    • These authors contributed equally to this work.

  • Chao Chen,

    1. Cancer Research Institute of Basic Medical School, Southern Medical University, Guangzhou, China
    2. Otorhinolaryngology of Zhujiang Hospital, Southern Medical University, Guangzhou, China
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    • These authors contributed equally to this work.

  • Huiling Yang,

    1. School of Pharmacy, Guangdong Medical College, Dongguan, PR China
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    • These authors contributed equally to this work.

  • Yajie Zhang,

    1. Department of Pathology, Basic School of Guangzhou Medical College, Guangzhou, China
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    • These authors contributed equally to this work.

  • Jie Long,

    1. Department of Pathology, Basic School of Guangzhou Medical College, Guangzhou, China
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  • Xiaobin Long,

    Corresponding author
    • Otorhinolaryngology of Zhujiang Hospital, Southern Medical University, Guangzhou, China
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  • Weiyi Fang

    Corresponding author
    1. Cancer Research Institute of Basic Medical School, Southern Medical University, Guangzhou, China
    • Department of Pathology, Basic School of Guangzhou Medical College, Guangzhou, China
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  • Colour Online: See the article online to view Figs. 1, 3, 4 and 6 in colour.

Correspondence: Professor Weiyi Fang, Cancer Research Institute of Basic Medical School, Southern Medical University, Guangzhou 510515, China

E-mail: fangweiyi1975@yahoo.com.cn

Fax: +86-020-62789438

Additional corresponding author: Professor Xiaobin Long, E-mail: longfengxb@126.com

Abstract

We previously defined the recently revised NESG1 gene as a potential tumor suppressor in nasopharyngeal carcinoma (NPC). Here, we further used proteomics technology to globally examine NESG1-controlled proteins in NPC cells. Twenty-six proteins were found to be deregulated by NESG1 using proteomics analysis while enolase 1 (alpha) (ENO1), heat shock protein 90 kDa beta (Grp94), member 1 (HSP90B1), and cathepsin D (CTSD) proteins were differentially expressed by Western blot. Interestingly, a-enolase (ENO1), an overexpressed gene in NPC, was confirmed as a NESG1-regulated protein in NPC cells. Overexpressed ENO1 not only restored cell proliferation and cell-cycle progression, but also antagonized the regulation of NESG1 to cell-cycle regulators p21 and CCNA1 expression as well as induced the expression of C-Myc, pRB, and E2F1 in NESG1-ovexpressed NPC cells. Real-time PCR and immunohistochemistry analysis showed that NESG1 expression is negatively correlated with ENO1 expression in NPC tissues. Our observations suggest that ENO1 downregulation plays an important role in NESG1-induced growth inhibition of NPC cancer cells.

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