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Related Experiment Videos

Phorbol esters, but not epidermal growth factor or insulin, rapidly decrease soluble protein kinase C activity in rat

W J Vaartjes, C G de Haas, S G van den Bergh

    Biochemical and Biophysical Research Communications
    |August 14, 1986
    PubMed
    Summary
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    Tumor promoters like phorbol esters trigger protein kinase C (PKC) movement in rat hepatocytes. However, physiological growth factors such as insulin and EGF do not affect PKC, suggesting PKC is not essential for their metabolic actions.

    Area of Science:

    • Biochemistry
    • Cell Biology
    • Molecular Pharmacology

    Background:

    • Protein kinase C (PKC) is a family of enzymes involved in cell signaling.
    • Tumor promoters can activate signaling pathways in cells.
    • Physiological growth factors like insulin and epidermal growth factor (EGF) regulate cell metabolism.

    Purpose of the Study:

    • To investigate the effect of tumor-promoting phorbol esters on protein kinase C (PKC) localization in rat hepatocytes.
    • To determine if PKC activation is involved in the short-term metabolic actions of epidermal growth factor (EGF) and insulin.

    Main Methods:

    • Freshly isolated rat hepatocytes were exposed to phorbol 12-myristate 13-acetate (PMA), EGF, or insulin.
    • Cellular fractions (soluble and particulate) were isolated.

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  • Protein kinase C activity and translocation were measured.

    • Main Results:

    • Phorbol 12-myristate 13-acetate (PMA) induced a time- and concentration-dependent translocation of PKC from the soluble to the particulate fraction of hepatocytes.
    • Neither epidermal growth factor (EGF) nor insulin caused a significant disappearance of soluble PKC activity.
    • This indicates that PKC activation is not a common event in the early response to these growth factors.

    Conclusions:

    • Tumor promoters activate PKC in hepatocytes via translocation.
    • PKC activation is not required for the rapid metabolic effects of EGF and insulin on hepatocytes.
    • These findings differentiate the signaling pathways of tumor promoters from physiological growth factors.