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Adrenomedullin is a cross-talk molecule that regulates tumor and mast cell function during human carcinogenesis

  1. Author:
    Zudaire, E.
    Martinez, A.
    Garayoa, M.
    Pio, R.
    Kaur, G.
    Woolhiser, M. R.
    Metcalfe, D. D.
    Hook, W. A.
    Siraganian, R. P.
    Guise, T. A.
    Chirgwin, J. M.
    Cuttitta, F.

  2. Author Address

    NCI, CCBB, CCR, Bethesda, MD 20892 USA. CSIC, Dept Cell Biol & Neuroanat, Inst Cajal, Madrid, Spain. Univ Navarra, Dept Cellular & Pathol, E-31080 Pamplona, Spain. Univ Navarra, Dept Biochem, E-31080 Pamplona, Spain. NCI, Biol Testing Branch, Div Canc Treatment & Diag, Frederick Canc Res & Dev Ctr, Frederick, MD 21701 USA. NIAID, Lab Allerg Dis, Bethesda, MD 20892 USA. Natl Inst Dent & Craniofacial Res, Receptor & Signal Transduct Sect, Oral Infect & Immunol Branch, Bethesda, MD USA. Univ Virginia Hlth Syst, Dept Internal Med, Div Endocrinol, Charlottesville, VA USA Zudaire, E, NCI, CCBB, CCR, Bldg 10,Rm 12N226, Bethesda, MD 20892 USA
    1. Year: 2006
    2. Date: JAN
  2. Journal: American Journal of Pathology
    1. 168
    2. 1
    3. Pages: 280-291
  4. Type of Article: Article
  1. Abstract:

    We have previously demonstrated that adrenomedullin (AM) plays a critical role as an autocrine/paracrine tumor cell survival factor. We now present evidence that AM is an important regulator of mast cell (MC) function and that this modulation is potentially involved in tumor promotion. AM induced histamine or P-hexosaminidase release from rat and human MCs through a receptor-independent pathway. AM was chemotactic for human MCs and stimulated mRNA expression of vascular endothelial growth factor, monocyte chemoattractant protein-1, and basic fibroblast growth factor in this cell type. Differentiated but not undifferentiated human MCs responded to hypoxic insult with elevated AM mRNA/protein expression. Using confocal microscopy, we identified AM-producing MCs in tumor infiltrates of human breast and lung cancer patients. in mixed culture assays both anchorage-dependent and -independent growth of human lung cancer A549 cells, an effect that was suppressed by MC-targeted siRNA AM knockdown. Finally, HMC-1 cells induced in vivo angiogenesis as assessed by directed in vivo angiogenesis assay analysis; neutralizing anti-AM monoclonal antibody blocked this ability. Our collective data suggest a new role for AM as a cross-talk molecule that integrates tumor and MC communication, underlying a unique promotion mechanism of human cancers

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External Sources

  1. View record in Web of Science®
  2. WOS: 000234449400030

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