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Co-operative functions between nuclear factors NF kappa B and CCAT/enhancer-binding protein-beta (C/EBP-beta) regulate the IL-6 promoter in autocrine human prostate cancer cells

  1. Author:
    Xiao, W. H.
    Hodge, D. R.
    Wang, L. H.
    Yang, X. Y.
    Zhang, X. H.
    Farrar, W. L.

  2. Author Address

    NCI, Basic Res Program, SAIC Frederick, Mol Immunoregulat Lab,Canc Res & Dev Ctr,NIH, Frederick, MD 21702 USA. NCI, Cytokine Mol Mech Sect, Mol Immunoregulat Lab, Canc Res & Dev Ctr,NIH, Frederick, MD 21702 USA Farrar, WL, NCI, Basic Res Program, SAIC Frederick, Mol Immunoregulat Lab,Canc Res & Dev Ctr,NIH, POB B,Bldg 560,Rm 31-76, Frederick, MD 21702 USA
    1. Year: 2004
    2. Date: DEC 1
  2. Journal: Prostate
    1. 61
    2. 4
    3. Pages: 354-370
  4. Type of Article: Article
  1. Abstract:

    BACKGROUND. IL-6 is a growth and survival factor for prostate cancer cells through autocrine pathways. Here, we have systematically examined the transcriptional regulation mechanisms of IL-6 in autocrine prostate cancer cells.METHODS. RT-PCR and immunohistochemical staining were used to determine IL-6 production in the cells. Serial mutant IL-6 promoter luciferase reporters were generated and their transcriptional activities were examined. The transcription factors involved in IL-6 regulation were identified with super-shift EMSA. Overexpression of NFKB p65 and C/EBP-P, and blockade of NFKB with IKBalpha or CAPE were performed to demonstrate the cooperation between NFKB p65 and C/EBP-beta in activation of IL-6.RESULTS. Transcription factor regulatory sites IL6-NFKB, IL6-C/EBP, IL6-CREB, and IL6AP1, are responsive to constitutively activated IL-6 production in autocrine prostate cancer cell lines. Among these sites, IL6-AP1 and IL6-C/EBP appear most important, while IL6-NFKB shows the least effect for IL-6 promoter activity as determined by mutant IL-6 promoter luciferase reporter assay. Nevertheless, nuclear factor NFKB is activated and required. Such activation is minimally dependent upon the IL6-NFKB site, occurring through cooperation with other transcription factors that bind the IL-6 promoter. Cooperation between NFKB p65 and C/ EBP-beta did not require a functional IL6-NFKB binding site

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  1. View record in Web of Science®
  2. WOS: 000225153200006

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