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Cyclic AMP in ovarian cancer cells both inhibits proliferation and increases c-KIT expression

Tanya J Shaw1, Eniko J Keszthelyi, Angela M Tonary

  • 1Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Ontario K1H 1C4, Canada.

Experimental Cell Research
|February 14, 2002
PubMed

Insights

Cyclic AMP (cAMP) inhibits ovarian cancer cell proliferation and upregulates c-KIT expression. However, the KIT receptor tyrosine kinase is not responsible for this observed anti-proliferative effect in ovarian cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • C-KIT (KIT) receptor tyrosine kinase and its ligand (KL) are coexpressed in over 70% of epithelial ovarian cancers.
  • Cyclic AMP (cAMP) signaling is known to inhibit cancer cell proliferation but can also upregulate KIT and KL expression.

Purpose of the Study:

  • To confirm cAMP's growth inhibitory effects on ovarian cancer cells.
  • To investigate cAMP's impact on c-KIT and KL expression in ovarian cancer.
  • To examine the role of cAMP-regulated KIT/KL in ovarian cancer cell proliferation.

Main Methods:

  • Ovarian cancer HEY cells were treated with cAMP-elevating agents (dbcAMP, 8-bromo-cAMP, cholera toxin).
  • c-KIT and KL mRNA expression levels were quantified using quantitative PCR.
  • The effect of KIT inhibition (using neutralizing antibodies or STI571) on proliferation was assessed.

Main Results:

  • cAMP stimulation dose-dependently inhibited HEY cell proliferation by up to 62%.
  • cAMP treatment increased c-KIT mRNA expression 4- to 7-fold, without affecting KL mRNA.
  • Inhibition of KIT activity did not reverse the cAMP-induced anti-proliferative effect.

Conclusions:

  • cAMP signaling pathways regulate both ovarian cancer cell proliferation and c-KIT expression.
  • The KIT receptor tyrosine kinase is not the mediator of cAMP's anti-proliferative effects in these ovarian cancer cells.

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