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J.Health Sci., 50(3), 271-276, 2004
Cytotoxicity of Clinically-Used Non-Steroidal
Anti-Inflammatory Drugs (NSAIDs) in the Human Bladder Cancer Cell
Line UM-UC-3
Fumihiko Kugawa,* Kazuo Ide, and Masatada Aoki
Department of Biological Pharmaceutical Sciences, College of
Pharmacy, Nihon University, 7-7-1 Narashino-dai, Funabashi,
Chiba 274-8555, Japan
We evaluated 8 clinically-used non-steroidal anti-inflammatory drugs (NSAIDs): Aspirin,
Etodolac, Diclofenac, Ibuprofen, Indomethacin, Mefenamic acid, Nabumetone, and Piroxicam, for
cytotoxicity in the human bladder cancer cell line
UM-UC-3 in vitro. Basing our dosages on the
maximum concentration of each NSAID used clinically,
four concentrations of each drug were prepared, and
the viability of UM-UC-3 cells given each
treatment was monitored for up to 5 days. At the
highest concentration, Aspirin and Diclofenac caused
no decrease in UM-UC-3 viability during the 5-day
incubation. Etodolac, Ibuprofen, Indomethacin, and
Piroxicam decreased the viability of UM-UC-3 cells
about 20% on the fifth day. Treatment with
30 mu g/ml of Mefenamic acid and
16 mu g/ml of Nabumetone caused about a 40% loss of cell viability on the last
day of the experiment. Thus, the most effective
cytotoxicity was observed with Mefenamic acid and
Nabumetone. We then examined the nature of the cell death induced by these two drugs, by
biochemical and morphological analyses. A DNA
fragmentation assay showed DNA-ladder formation with
both Mefenamic acid and Nabumetone treatment. In addition, nuclear blebbing was observed by
fluorescence microscopy in both Mefenamic acid- and
Nabumetone-treated cells. Since DNA ladder formation and nuclear blebbing are hallmarks of
typical apoptotic cell death, we concluded that at least
two NSAIDs, Mefenamic acid and Nabumetone, could cause apoptotic cell death in the human
bladder cell line, UM-UC-3.
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