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Nimesulide and indomethacin induce apoptosis in head and neck cancer cells
Author(s) -
Pelzmann Martina,
Thurnher Dietmar,
Gedlicka Claudia,
Martinek Helga,
Knerer Birgit
Publication year - 2004
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/j.1600-0714.2004.00216.x
Subject(s) - nimesulide , apoptosis , head and neck squamous cell carcinoma , carcinogenesis , cyclooxygenase , cell , cancer research , cell culture , cancer , gene isoform , blot , cancer cell , programmed cell death , cell growth , medicine , enzyme , chemistry , pharmacology , biology , head and neck cancer , biochemistry , gene , genetics
Background: Non‐steroidal anti‐inflammatory drugs (NSAIDs) are known to inhibit the enzyme cyclooxygenase (COX). There are two isoforms of the enzyme. Recent investigations indicate that both isoforms, COX‐1 and COX‐2, are involved in carcinogenesis. Methods: We investigated the effects of nimesulide, a COX‐2 selective and indomethacin, a non‐selective NSAID on the head and neck squamous cell carcinoma (HNSCC) cell lines SCC‐9 and SCC‐25. Effects on cell numbers and apoptosis were assayed by cell counting, immunofluorescence and fluorescence activated cell sorting (FACS). COX expression was examined by Western blotting. Results: The investigated cell lines express COX‐1 and COX‐2. Nimesulide and indomethacin induce apoptosis and cause a reduction of cell number. Incubation with NSAIDs upregulated COX‐2 expression. Conclusion: The results of our study on HNSCC cells together with data from different studies showing anti‐cancer activity of NSAIDs suggest that COX inhibitors could play a role in HNSCC treatment and prevention.