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Two independent growth factor-generated signals regulate c-fos and c-myc mRNA levels in Swiss 3T3 cells

P McCaffrey, W Ran, J Campisi

    The Journal of Biological Chemistry
    |February 5, 1987
    PubMed

    Insights

    Epidermal growth factor (EGF) and phosphatidylinositol (PI) turnover signaling pathways activate proto-oncogenes c-myc and c-fos through distinct mechanisms. This research clarifies distinct signaling routes for growth factor-induced gene expression.

    Area of Science:

    • Cellular signaling and molecular biology
    • Cancer research and oncogenesis
    • Gene expression regulation

    Background:

    • Polypeptide growth factors stimulate cell proliferation via cell surface receptors and intracellular pathways.
    • Phosphatidylinositol (PI) turnover and protein kinase C activation are key signaling events.
    • Certain growth factors, like mitogens, rapidly increase proto-oncogenes c-myc and c-fos expression.

    Purpose of the Study:

    • To elucidate the distinct signal transduction pathways responsible for proto-oncogene activation.
    • To investigate the role of protein kinase C in mediating growth factor-induced c-myc and c-fos expression.
    • To differentiate the signaling mechanisms of epidermal growth factor (EGF) versus PI turnover-stimulating factors.

    Main Methods:

    • Swiss 3T3 cells were treated with phorbol dibutyrate to deplete protein kinase C.
    • Cells were subsequently stimulated with platelet extract, bombesin, or EGF.
    • Messenger RNA (mRNA) levels for c-myc and c-fos were quantified.

    Main Results:

    • Platelet extract and bombesin showed weaker induction of c-myc and c-fos mRNA in protein kinase C-depleted cells.
    • Epidermal growth factor (EGF) potently induced c-myc and c-fos mRNA regardless of protein kinase C status.
    • EGF and PI turnover-stimulating factors utilize different pathways for proto-oncogene induction.

    Conclusions:

    • EGF and growth factors activating PI turnover induce c-myc and c-fos proto-oncogenes via separate signaling cascades.
    • Protein kinase C is involved in the signaling pathway for PI turnover-dependent proto-oncogene activation.
    • Distinct molecular mechanisms govern growth factor-mediated proto-oncogene expression.

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