Dual inhibition of cyclooxygenase-2 and soluble epoxide hydrolase synergistically suppresses primary tumor growth and metastasis

Proc Natl Acad Sci U S A. 2014 Jul 29;111(30):11127-32. doi: 10.1073/pnas.1410432111. Epub 2014 Jul 14.

Abstract

Prostaglandins derived from the cyclooxygenase (COX) pathway and epoxyeicosatrienoic acids (EETs) from the cytochrome P450/soluble epoxide hydrolase (sEH) pathway are important eicosanoids that regulate angiogenesis and tumorigenesis. COX-2 inhibitors, which block the formation of prostaglandins, suppress tumor growth, whereas sEH inhibitors, which increase endogenous EETs, stimulate primary tumor growth and metastasis. However, the functional interactions of these two pathways in cancer are unknown. Using pharmacological inhibitors as probes, we show here that dual inhibition of COX-2 and sEH synergistically inhibits primary tumor growth and metastasis by suppressing tumor angiogenesis. COX-2/sEH dual pharmacological inhibitors also potently suppress primary tumor growth and metastasis by inhibiting tumor angiogenesis via selective inhibition of endothelial cell proliferation. These results demonstrate a critical interaction of these two lipid metabolism pathways on tumorigenesis and suggest dual inhibition of COX-2 and sEH as a potential therapeutic strategy for cancer therapy.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Antineoplastic Agents
  • Cyclooxygenase 2 / metabolism*
  • Cyclooxygenase 2 Inhibitors / pharmacology*
  • Drug Synergism
  • Epoxide Hydrolases* / antagonists & inhibitors
  • Epoxide Hydrolases* / metabolism
  • Male
  • Mice
  • Neoplasm Metastasis
  • Neoplasm Proteins / agonists
  • Neoplasm Proteins / antagonists & inhibitors
  • Neoplasm Proteins / metabolism
  • Neoplasm Proteins / pharmacology*
  • Neoplasms, Experimental* / drug therapy
  • Neoplasms, Experimental* / enzymology
  • Neoplasms, Experimental* / pathology

Substances

  • Antineoplastic Agents
  • Cyclooxygenase 2 Inhibitors
  • Neoplasm Proteins
  • Ptgs2 protein, mouse
  • Cyclooxygenase 2
  • Epoxide Hydrolases