Indomethacin decreases EP2 prostanoid receptor expression in colon cancer cells

Hiromichi Fujino, Xiao bo Chen, John W. Regan, Toshihiko Murayama

Research output: Contribution to journalArticlepeer-review

29 Scopus citations


Nonsteroidal anti-inflammatory drugs (NSAIDs) can decrease the risk of colorectal cancer; however, it has not been established if this effect is solely through their ability to inhibit cyclooxygenase (COX). In this study the effects of indomethacin, a potent NSAID and nonselective COX inhibitor, was examined in LS174T human colon cancer cells. These cells were found to express EP2 prostanoid receptors, but not the EP1, EP3 or EP4 subtypes. Pretreatment of LS174T cells with indomethacin produced a complete inhibition of prostaglandin E2 (PGE2) stimulated cyclic AMP (cAMP) formation in a dose dependent manner with an IC50 of 21 μM. Interestingly, the inhibition of PGE2-stimulated cAMP formation by indomethacin was accompanied by a decrease in EP2 mRNA expression and by a decrease in the whole cell specific binding of [3H]PGE2. Thus, treatment of LS174T cells with indomethacin causes a down regulation of EP2 prostanoid receptors expression that may be independent of COX inhibition.

Original languageEnglish (US)
Pages (from-to)568-573
Number of pages6
JournalBiochemical and Biophysical Research Communications
Issue number3
StatePublished - Aug 3 2007


  • EP2 receptor
  • G-protein coupled receptors
  • Indomethacin
  • LS174T cells
  • NSAIDs
  • PGE
  • Prostaglandin E
  • cAMP

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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