Oncogene Functions of FHL2 Are Independent from NF-κBIα in Gastrointestinal Cancer
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  • 作者:Liang Qiao (1)
    Yan Wang (1)
    Roberta Pang (1)
    Jide Wang (1)
    Yun Dai (1)
    Juan Ma (1)
    Qing Gu (1)
    Zesong Li (1)
    Yusheng Zhang (1)
    Bing Zou (1)
    H. Y. Lan (1)
    Benjamin C. Y. Wong (1) (2)
  • 关键词:FHL2 ; NF ; κB ; NF ; κBIα ; Interaction ; Gastric cancer ; Colon cancer
  • 刊名:Pathology & Oncology Research
  • 出版年:2009
  • 出版时间:March 2009
  • 年:2009
  • 卷:15
  • 期:1
  • 页码:31-36
  • 全文大小:185KB
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  • 作者单位:Liang Qiao (1)
    Yan Wang (1)
    Roberta Pang (1)
    Jide Wang (1)
    Yun Dai (1)
    Juan Ma (1)
    Qing Gu (1)
    Zesong Li (1)
    Yusheng Zhang (1)
    Bing Zou (1)
    H. Y. Lan (1)
    Benjamin C. Y. Wong (1) (2)

    1. Department of Medicine, The University of Hong Kong, Hong Kong, China
    2. Department of Medicine, University of Hong Kong, Queen Mary Hospital, Hong Kong, China
  • ISSN:1532-2807
文摘
Four and a half of LIM-only protein 2 (FHL2) is an adaptor protein that can interact with many transcription factors and thus plays a variety of biological functions. Previous studies by our group have demonstrated that suppression of FHL2 was capable of inducing tumor cell differentiation, and inhibiting the growth of experimental gastric and colon cancers. Therefore, FHL2 appears to function as an oncogene. In order to further explore the mechanisms of how FHL2 is involved in tumorigenesis, we attempted to test whether FHL2 has any direct association with nuclear factor (NF-κB), the most important transcription factor involved in apoptosis, inflammation, and carcinogenesis. Using an Yeast Two Hybrid (Y2H) screening system, we have shown that FHL2 may have an interaction with NF-κBIα, the coding gene for IκBα which is the most potent endogenous inhibitor for NF-κB activation. However, subsequent studies using co-immunoprecipitation and co-localization failed to confirm the Y2H finding. Down-regulation of FHL2 by FHL2-siRNA down-regulated the expression of NF-κB p65. We therefore concluded that under the physiological condition, FHL2 may activate NF-κB pathway, even though such an activation may not be mediated by a direct binding of FHL2 to NF-κB inhibitor protein IκB.

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