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Targeting prostaglandin E EP receptors to inhibit metastasis

Amy M Fulton1, Xinrong Ma, Namita Kundu

  • 1Department of Pathology and Marlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA. afulton@umaryland.edu

Cancer Research
|October 19, 2006
PubMed

Insights

Targeting prostaglandin E2 (PGE2) signaling, specifically the EP4 receptor, effectively inhibits experimental metastasis in breast cancer. This offers a promising alternative to COX-2 inhibitors for treating aggressive malignancies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • High cyclooxygenase-2 (COX-2) expression correlates with aggressive behavior in breast and other cancers.
  • Concerns exist regarding the safety of long-term COX-2 inhibitor use and the need for better metastatic disease treatments.

Purpose of the Study:

  • To test if inhibiting prostaglandin E2 (PGE2) downstream signaling is as effective as inhibiting global prostaglandin synthesis for cancer treatment.
  • To investigate the role of specific E-series of prostaglandin (EP) receptors in cancer progression.

Main Methods:

  • Summarizing existing laboratory data on EP receptor roles in cancer.
  • Presenting new findings on EP4 receptor antagonists in a murine model of hormone-resistant, metastatic breast cancer.

Main Results:

  • EP4 receptor antagonists demonstrated inhibition of experimental metastasis in a murine breast cancer model.
  • Selective targeting of individual EP receptors shows potential for exploiting high COX-2 activity in epithelial malignancies.

Conclusions:

  • Inhibiting PGE2 downstream signaling via EP4 receptor antagonism is a viable strategy for combating metastatic breast cancer.
  • Further investigation into selective EP receptor targeting is warranted for treating COX-2-driven epithelial malignancies.

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