Cyclooxygenase inhibitors induce apoptosis in oral cavity cancer cells by increased expression of nonsteroidal anti-inflammatory drug-activated gene

Biochem Biophys Res Commun. 2004 Dec 24;325(4):1298-303. doi: 10.1016/j.bbrc.2004.10.176.

Abstract

We have investigated whether NAG-1 is induced in oral cavity cancer cells by various NSAIDs and if apoptosis induced by NSAIDs can be linked directly with the induction of NAG-1. NAG-1 expression was increased by diclofenac, aceclofenac, indomethacin, ibuprofen, and sulindac sulfide, in the order of NAG-1 induction, but not by acetaminophen, piroxicam or NS-398. Diclofenac was the most effective NAG-1 inducer. Incubation with diclofenac inhibited cell proliferation and induced apoptosis. The expression of NAG-1 was observed in advance of the induction of apoptosis. Conditioned medium from NAG-1-overexpressing Drosophila cells inhibited SCC 1483 cells proliferation and induced apoptosis. In summary, some NSAIDs induce NAG-1 expression in oral cavity cancer cells and the induced NAG-1 protein appears to mediate apoptosis. Therefore, NSAIDs may be considered as a possible chemopreventive agent against oral cavity cancer.

Publication types

  • Comparative Study

MeSH terms

  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology*
  • Antineoplastic Agents / pharmacology
  • Apoptosis / drug effects*
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cyclooxygenase Inhibitors / pharmacology*
  • Cytokines / metabolism*
  • Cytokines / pharmacology*
  • Dose-Response Relationship, Drug
  • Growth Differentiation Factor 15
  • Humans
  • Mouth / drug effects
  • Mouth / pathology
  • Mouth Neoplasms / metabolism*
  • Mouth Neoplasms / pathology*
  • Recombinant Proteins / metabolism
  • Recombinant Proteins / pharmacology

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Antineoplastic Agents
  • Cyclooxygenase Inhibitors
  • Cytokines
  • GDF15 protein, human
  • Growth Differentiation Factor 15
  • Recombinant Proteins