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Reduced receptor expression for platelet-derived growth factor and epidermal growth factor in dividing mouse lung epithelial cells

  1. Author:
    Rice, P. L.
    Porter, S. E.
    Koski, K. M.
    Ramakrishna, G.
    Chen, A.
    Schrump, D.
    Kazlauskas, A.
    Malkinson, A. M.
  2. Author Address

    Malkinson AM Univ Colorado, Hlth Sci Ctr, Sch Pharm, Dept Pharmaceut Sci 4200 E 9th Ave,Campus Box C238 Denver, CO 80262 USA Univ Colorado, Hlth Sci Ctr, Sch Pharm, Dept Pharmaceut Sci Denver, CO 80262 USA NCI, Frederick Canc Res & Dev Ctr, Comparat Carcinogenesis Lab Frederick, MD 21702 USA NCI, Surg Branch, Thorac Oncol Sect Bethesda, MD 20892 USA Harvard Univ, Sch Med, Schepens Eye Res Inst Boston, MA 02115 USA
    1. Year: 1999
  1. Journal: Molecular Carcinogenesis
    1. 25
    2. 4
    3. Pages: 285-294
  2. Type of Article: Article
  1. Abstract:

    The roles of growth factors in mouse lung neoplasia were investigated by examining receptors for platelet-derived growth factor (PDGF) and epidermal growth factor (EGF) in epithelial cell lines. Whereas nontumorigenic lung cells expressed mRNA and protein for PDGF receptor (PDGFR)-alpha, PDGFR-beta, and EGF receptor (EGFR), five of six neoplastic lines did not. Because this exceptional tumorigenic cell line grows slowly, we hypothesized that receptor levels increased with cell stasis. To test this hypothesis, serum concentrations were manipulated, and log-phase and postconfluent cells were compared. Consistent with our hypothesis, PDGFR-alpha and EGFR contents, but not PDGFR-beta contents, increased at stasis. Ki-ras mutation initiates lung tumorigenesis in mice, but activation of Ki-ras did not affect receptor expression. This was determined both by transfecting nontumorigenic cells with activated Ki-ras and neoplastic cells with a Ki-ras antisense construct and by diminishing Ki-ras activation by using a farnesyltransferase inhibitor. Stasis-associated upregulation of growth-factor receptor expression suggests a function in lung cell differentiation that is abrogated during neoplastic growth. (C) 1999 Wiley-Liss, Inc. [References: 53]

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