Dual Effect of Flurbiprofen on Cell Proliferation and Agonist‐Induced Ca2+ Movement in Human Osteosarcoma Cells

• Published in: Basic & clinical pharmacology & toxicology 2006-02, Vol.98 (2), p.160-167
• Main Authors: Tseng, Li‐Ling, Cheng, He‐Hsiung, Huang, Chun‐Jen, Liu, Shiuh‐Inn, Kuo, Chun‐Chi, Chen, Wei‐Chuan, Huang, Jong‐Khing, Hsu, Shu‐Shong, Chang, Hong‐Tai, Kao, Cheng‐Hsing, Ho, Chin‐Man, Jan, Chung‐Ren
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; Diseases of the osteoarticular system; Medical sciences; Pharmacology. Drug treatments; Tumors of striated muscle and skeleton
• ISSN: 1742-7835; 1742-7843
• DOI: 10.1111/j.1742-7843.2006.pto_279.x

: In human MG63 osteosarcoma cells, the effect of flurbiprofen on intracellular Ca2+ concentrations ([Ca2+]i) and proliferation was explored. The proliferation was enhanced by 20–120 μM flurbiprofen, and was decreased by 140–200 μM flurbiprofen. The effect of flurbiprofen on the increases in cytosolic free Ca2+ levels ([Ca2+]i) induced by ATP, bradykinin, histamine and thapsigargin (an inhibitor of the endoplasmic reticulum Ca2+ ATPase), was examined. In cell preincubated with 20 or 80 μM flurbiprofen, the [Ca2+]i increases induced by all agonists were attenuated. In the presence of 20 μM flurbiprofen, the decreased [Ca2+]i responses with the agonists were attributed to a defective Ca2+ influx because this decrease was unobserved in agonists‐induced [Ca2+]i increases in the absence of extracellular Ca2+. In the presence of 80 μM flurbiprofen, both the Ca2+ influx component and the Ca2+ releasing (from organelles) component were defective. These results suggest that flurbiprofen could alter proliferation and inhibit [Ca2+]i increases.