In ovarian cancer, the molecular targeted chemotherapeutics could increase the efficiency of low-dose radiotherapy while decreasing injury to adjusted organs. In irradiated A2780 human ovarian carcinoma cells, cytosolic phospholipase A2 (cPLA2) inhibitor AACOCF3 prevented activation of pro-survival Akt signaling and enhanced cell death. The potential molecular mechanisms of this effect could involve signaling through lysophosphatidic acid receptors. In the heterotopic A2780 tumor model using nude mice, cPLA2 inhibition significantly delayed tumor growth compared to treatment with radiation or vehicle alone. These results identify cPLA2 as a molecular target to enhance the therapeutic ratio of radiation in ovarian cancer.

Original languageEnglish
Pages (from-to)137-143
Number of pages7
JournalCancer Letters
Issue number2
StatePublished - May 28 2011


  • Cytosolic phospholipase A2
  • Lysophosphatidic acid
  • Lysophosphatidylcholine
  • Ovarian cancer
  • Radiation therapy


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