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J Dent Res ; 88(2): 164-9, 2009 Feb.
Article in English | MEDLINE | ID: mdl-19278989

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.


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