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Suppression of TNF-alpha mediated apoptosis by EGF in TNF-alpha sensitive human cervical carcinoma cell line

Hakan Akca1, Selma Yenisoy Akan, Atila Yanikoglu

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

Growth Factors (Chur, Switzerland)
|June 11, 2003
PubMed

Insights

Human epidermal growth factor (EGF) protects cervical cancer cells from tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis by activating protein kinase C-delta (PKC-delta). This pathway regulates p53 and p21 levels, crucial in cancer suppression.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • The tumor suppressor protein p53 plays a critical role in guarding against oncogenic stress and DNA damage.
  • Cancer cells often secrete growth factors that promote survival and inhibit apoptosis.
  • Understanding the interplay between growth factors and cell death pathways is crucial for cancer therapy.

Purpose of the Study:

  • To investigate the effects of human epidermal growth factor (EGF) on tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis in human cervical carcinoma cells (ME180S).
  • To elucidate the specific kinase pathway involved in EGF's suppressive effects on TNF-alpha-mediated apoptosis.
  • To determine the role of protein kinase C (PKC) subtypes in mediating EGF's protective action.

Main Methods:

  • Treatment of ME180S cells with TNF-alpha and/or EGF.
  • Assessment of p53 and p21 protein levels via Western blotting.
  • Evaluation of apoptosis induction using cell viability assays.
  • Inhibition of specific kinase pathways (MAPK, PI3K, PKC) using chemical inhibitors.
  • Analysis of PKC-delta activation and translocation using immunofluorescence.

Main Results:

  • TNF-alpha treatment increased cellular levels of p53 and p21, inducing apoptosis in ME180S cells.
  • Pretreatment with EGF suppressed TNF-alpha-induced p53 and p21 accumulation and apoptosis.
  • Inhibition of PKC pathways reversed EGF's suppressive effects, implicating PKC in the mechanism.
  • EGF treatment specifically activated PKC-delta, causing its redistribution from the cytosol to the membrane.
  • PKC inhibition (GF 109203X) blocked EGF-mediated suppression of TNF-alpha effects.

Conclusions:

  • EGF protects ME180S cervical carcinoma cells from TNF-alpha-induced apoptosis.
  • This protective effect is mediated through the activation of the PKC-delta pathway.
  • The findings highlight a novel mechanism by which EGF influences cancer cell survival and apoptosis.

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