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IL-6 induces expression of the Fli-1 proto-oncogene via STAT3

  1. Author:
    Hodge, D. R.
    Li, D. P.
    Qi, S. M.
    Farrar, W. L.

  2. Author Address

    NCI, Frederick Canc Res & Dev Ctr, Mol Immunoregulat Lab, POB B,Bldg 560,Rm 31-76, Frederick, MD 21702 USA NCI, Frederick Canc Res & Dev Ctr, Mol Immunoregulat Lab, Frederick, MD 21702 USA NCI, Frederick Canc Res & Dev Ctr, SAIC Frederick, Intramural Res Support Program, Frederick, MD 21702 USA NCI, Frederick Canc Res & Dev Ctr, Cytokine Mol Mech Sect, Frederick, MD 21702 USA Aphton Corp, Mol Med Lab, Miami, FL 33130 USA Farrar WL NCI, Frederick Canc Res & Dev Ctr, Mol Immunoregulat Lab, POB B,Bldg 560,Rm 31-76, Frederick, MD 21702 USA
    1. Year: 2002
  2. Journal: Biochemical and Biophysical Research Communications
    1. 292
    2. 1
    3. Pages: 287-291
  4. Type of Article: Article
  1. Abstract:

    Induction of gene expression by IL-6 has become an area of intense interest due to the role this cytokine plays in mediating aspects of inflammation, cellular differentiation, and proliferation. The ETS family of transcription factors represents a group of positive and negative regulators of transcription, that are differentially expressed in a cell and tissue specific manner. The ETS protein Fli-I is known to induce differentiation in the erythroblastic leukemia cell line K562 along megakaryocytic developmental pathways. Here we show that IL-6 treatment of K562 induces the expression of Fli-1 via the STAT3 transcription factor. Upregulation of Fli-1 expression can be abrogated by the addition of AG490, a chemical inhibitor of JAK kinases, and by transfecting the cells with a dominant negative STAT3 expression construct.

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