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Epidermal growth factor suppresses interferon-induced accumulation of p53 and p21 by using protein kinase C

H Akca1, O N Ozes

  • 1Department of Biology, Faculty of Art and Science, Akdeniz University, Arapsuyu/Antalya, Turkey.

Scandinavian Journal of Clinical and Laboratory Investigation
|January 28, 2004
PubMed

Insights

Interferon alpha (IFN-alpha) and gamma (IFN-gamma) increase tumor suppressor p53 and p21 levels in ME180S cells. Epidermal growth factor (EGF) inhibits this effect through protein kinase C pathways.

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Cell Signaling

Background:

  • The tumor suppressor protein p53 is crucial for cellular defense against genomic damage and oncogenic stress.
  • p53 acts as a transcription factor, inducing cell-cycle arrest, senescence, or apoptosis upon activation.
  • Phosphorylation of p53 by kinases enhances its stability and nuclear localization, key steps in its tumor-suppressive function.

Purpose of the Study:

  • To investigate the effect of interferons (IFNs) on p53 and its target gene p21 expression in ME180S cells.
  • To determine the role of epidermal growth factor (EGF) and protein kinase C (PKC) pathways in modulating IFN-induced p53 and p21 accumulation.

Main Methods:

  • Treatment of ME180S cells with IFN-alpha and IFN-gamma.
  • Time-dependent analysis of p53 and p21 protein levels.
  • Pretreatment with EGF and assessment of its inhibitory effects on IFN-induced pathways.

Main Results:

  • IFN-alpha and IFN-gamma treatment led to a time-dependent increase in both p53 and p21 levels in ME180S cells.
  • Epidermal growth factor (EGF) pretreatment significantly inhibited the IFN-dependent induction of p53 and p21.
  • The inhibitory effect of EGF was mediated through protein kinase C (PKC) dependent pathways.

Conclusions:

  • Interferons effectively induce the tumor suppressor p53 and its downstream target p21 in ME180S cells.
  • EGF signaling, via PKC, can counteract the pro-apoptotic and cell-cycle arrest effects of IFNs by inhibiting p53 and p21 induction.
  • This highlights a complex interplay between growth factor and cytokine signaling in regulating p53-mediated tumor suppression.

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