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Transcriptional inactivation of STAT3 by PPAR gamma suppresses IL-6-responsive multiple myeloma cells

  1. Author:
    Wang, L. H.
    Yang, X. Y.
    Zhang, X. H.
    Huang, J. Q.
    Hou, J.
    Li, J.
    Xiong, H.
    Mihalic, K.
    Zhu, H. M.
    Xiao, W. H.
    Farrar, W. L.

  2. Author Address

    Wang, LH, Natl Canc Inst, Basic Res Program, SAIC Frederick, Frederick, MD 21702 USA Natl Canc Inst, Basic Res Program, SAIC Frederick, Frederick, MD 21702 USA. Natl Canc Inst, Cytoking Mol Mech Sect, Mol Immunoregulat Lab, Div Basic Sci, Frederick, MD 21702 USA. Mil Med Coll 2, Changzheng Hosp, Shanghai 200003, Peoples R China. Mil Med Coll 2, Xinhua Hosp, Shanghai 200003, Peoples R China.
    1. Year: 2004
  2. Journal: Immunity
    1. 20
    2. 2
    3. Pages: 205-218
  4. Type of Article: Article
  1. Abstract:

    Multiple myeloma (MM) remains largely incurable despite conventional and high-dose therapies. Therefore, novel biologically based treatment approaches are urgently required. Here we demonstrate that expression of peroxisome proliferator-activated receptor gamma (PPARgamma) in MM cells and its agonists 15-d-PGJ2 and troglitazone completely abolished IL-6-inducible MM cell proliferation and induced apoptosis through affecting expression of multiple cell cycle or apoptosis genes, whereas PPARgamma antagonist GW9662 and PPARalpha agonist WY14643 did not display this inhibitory effect. These PPARgamma agoinists significantly inhibited DNA binding and transactivation of STAT3 bound to the promoter of target genes in chromatin, but did not affect the expression of IL-6 receptor and phosphorylation of JAK/STAT3, MAPK, and PI3K/Akt. Interestingly, although inactivation of STAT3 by PPAR-y agonists is in a PPARgamma-dependent manner, the molecular mechanism by which two structurally distinct PPARgamma agonists suppress IL-6-activated STAT3 shows the divergent interactions between PPARgamma and STAT3 including direct or SMRT-mediated association

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