Indomethacin stimulates activity and expression of ecto-5'-nucleotidase/CD73 in glioma cell lines

Eur J Pharmacol. 2007 Aug 13;569(1-2):8-15. doi: 10.1016/j.ejphar.2007.04.058. Epub 2007 May 22.

Abstract

Gliomas are the most common and devastating primary tumors of the central nervous system. Ecto-NTPDases and ecto-5'-nucleotidase/CD73 can control extracellular ATP/adenosine levels, which have been described as proliferation factors. Here, we investigate the influence of indomethacin on the enzyme cascade that catalyses the interconversion of purine nucleotides in U138-MG and C6 glioma cell lines. Exposure of glioma cells to 100 microM indomethacin for 48 h caused increases of 52% (P < 0.05) and 62% (P < 0.05) in the AMP hydrolysis rate in C6 and U138-MG cell lines, respectively. Indomethacin treatments also increased ATP hydrolysis. Significant increase in ecto-5'-nucleotidase/CD73 mRNA and protein levels were observed after treatment with indomethacin. Pretreatment of glioma cells with a specific antagonist of the adenosine A(3) receptor, MRS1220 (1 microM; 9-Chloro-2-(2-furanyl)-5-((phenylacetyl)amino)-[1,2,4]triazolo[1,5-c]quinazoline), significantly reduced the inhibition of cell proliferation induced by indomethacin. In addition, a significant increase in mRNA levels of the adenosine A(3) receptor was observed after treatment with indomethacin. In conclusion, our data indicate that adenosine A(3) receptors and the enzyme, ecto-5'-nucleotidase/CD73, are involved in the anti-proliferative effect of indomethacin in glioma cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 5'-Nucleotidase / genetics*
  • 5'-Nucleotidase / metabolism
  • Actins / metabolism
  • Adenosine Diphosphate / analogs & derivatives
  • Adenosine Diphosphate / metabolism
  • Adenosine Monophosphate / metabolism
  • Adenosine Triphosphate / analogs & derivatives
  • Adenosine Triphosphate / metabolism
  • Adenosine Triphosphate / pharmacology
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Dimethyl Sulfoxide / pharmacology
  • Dose-Response Relationship, Drug
  • Enzyme Activation / drug effects
  • Flow Cytometry
  • Gene Expression Regulation, Enzymologic / drug effects
  • Glioma / enzymology
  • Glioma / genetics
  • Glioma / pathology
  • Humans
  • Indomethacin / pharmacology*
  • Purinergic P1 Receptor Agonists
  • Purinergic P1 Receptor Antagonists
  • Quinazolines / pharmacology
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Theophylline / analogs & derivatives
  • Theophylline / pharmacology
  • Time Factors
  • Triazoles / pharmacology
  • Xanthines / pharmacology

Substances

  • 9-chloro-2-(2-furyl)-5-phenylacetylamino(1,2,4)triazolo(1,5-c)quinazoline
  • Actins
  • Anti-Inflammatory Agents, Non-Steroidal
  • Purinergic P1 Receptor Agonists
  • Purinergic P1 Receptor Antagonists
  • Quinazolines
  • RNA, Messenger
  • Triazoles
  • Xanthines
  • 8-cyclopentyl-1,3-dimethylxanthine
  • Adenosine Monophosphate
  • Adenosine Diphosphate
  • Adenosine Triphosphate
  • 1,3-dipropyl-8-cyclopentylxanthine
  • Theophylline
  • 5'-Nucleotidase
  • alpha,beta-methyleneadenosine 5'-triphosphate
  • Indomethacin
  • Dimethyl Sulfoxide