Etodolac, a selective cyclooxygenase-2 inhibitor, induces apoptosis by activating caspases in human malignant rhabdoid tumor cells (FRTK-1)

Oncol Rep. 2007 Jan;17(1):169-73.

Abstract

Malignant rhabdoid tumor (MRT) is a rare and highly aggressive tumor presenting in the kidney and soft tissue in childhood. However, effective treatment for MRT has not been established. We investigated the antitumor effect of etodolac, a selective cyclooxygenase-2 inhibitor, on MRT cells in vitro using the MRT cell line FRTK-1. Etodolac induced apoptosis of FRTK-1 cells through activation of caspase-8, -9 and -3. Moreover, several caspase inhibitors completely or partially inhibited etodolac-induced apoptosis. Our data indicated that etodolac had an antitumor effect on MRT cells and holds promise as a novel therapeutic strategy for MRT.

MeSH terms

  • Amino Acid Chloromethyl Ketones / pharmacology
  • Apoptosis / drug effects*
  • Apoptosis / physiology
  • Caspases / metabolism*
  • Cell Line, Tumor
  • Cyclooxygenase 2 Inhibitors / pharmacology*
  • Cysteine Proteinase Inhibitors / pharmacology
  • Enzyme Activation / drug effects
  • Etodolac / pharmacology*
  • Humans
  • Isoenzymes / metabolism
  • Rhabdoid Tumor / drug therapy*
  • Rhabdoid Tumor / enzymology
  • Rhabdoid Tumor / pathology

Substances

  • Amino Acid Chloromethyl Ketones
  • Cyclooxygenase 2 Inhibitors
  • Cysteine Proteinase Inhibitors
  • Isoenzymes
  • benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone
  • Etodolac
  • Caspases