PGE2 production in oral cancer cell lines is COX-2-dependent

J Dent Res. 2009 Feb;88(2):164-9. doi: 10.1177/0022034508329519.

Abstract

It has been suggested that epithelial cyclooxygenase-2 (COX-2) promotes oral carcinogenesis and carcinoma malignancy through increased prostaglandin E(2) (PGE(2)) production. Although oral squamous cell carcinomas (OSCC) often express COX-2, they may also produce PGE(2) in a COX-1-dependent manner. We used 6 isolated cell lines to investigate which COX isoforms OSCC may use for PGE(2) production. COX-1 and -2 expression patterns divided the 6 OSCC cell lines into 3 distinct groups: both COX isoforms low, only COX-1 high, or both COX isoforms high. Multicolor immunohistofluorescence staining confirmed the COX-expression profiles in organotypic 3D cultures and the COX-2 dominance in OSCC tumors. Epidermal growth factor (EGF) stimulation induced COX-2 (but not COX-1) expression and increased PGE(2) production, which was attenuated by COX-2 (but not COX-1) specific inhibition or siRNA-mediated COX-2 gene knockdown. Thus, PGE(2) production in OSCC cell lines was COX-2-dependent.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Carcinoma, Squamous Cell / metabolism*
  • Cell Line, Tumor
  • Cyclooxygenase 1 / metabolism
  • Cyclooxygenase 2 / metabolism*
  • Cyclooxygenase Inhibitors / pharmacology
  • Dinoprostone / biosynthesis*
  • Dinoprostone / genetics
  • Epidermal Growth Factor / pharmacology
  • Female
  • Gene Expression / drug effects
  • Gene Knockdown Techniques
  • Humans
  • Intramolecular Oxidoreductases / biosynthesis
  • Isoenzymes / biosynthesis
  • Male
  • Middle Aged
  • Mouth Neoplasms / metabolism*
  • Prostaglandin-E Synthases
  • RNA, Small Interfering / pharmacology

Substances

  • Cyclooxygenase Inhibitors
  • Isoenzymes
  • RNA, Small Interfering
  • Epidermal Growth Factor
  • Cyclooxygenase 1
  • Cyclooxygenase 2
  • Intramolecular Oxidoreductases
  • Prostaglandin-E Synthases
  • Dinoprostone