| Cyclin-mediated G1 arrest by celecoxib differs in low-versus high-grade bladder cancer - Abstract |
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| Friday, 06 November 2009 | ||
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Department of Urology, William S. Middleton Memorial Veterans Hospital, and Department of Urology, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792, USA. This email address is being protected from spam bots, you need Javascript enabled to view it Celecoxib and other non-steroidal anti-inflammatory drugs (NSAIDs) are being evaluated in the prevention of bladder and other cancers. Here we investigate molecular effects of celecoxib independent of cyclooxygenase (COX)-2 expression levels in urothelial carcinoma of the bladder. Low-grade RT-4 and high-grade UM-UC-3 bladder cancer cells were treated with 0-50 muM celecoxib. Growth, cell cycle and apoptosis were measured by crystal violet elution and flow cytometry. Western analysis was performed for COX-2, Rb, cyclin B1/D1, and phospho-cyclin B1/D1. COX-2 induction was achieved with phorbol ester. Celecoxib inhibited growth of RT-4 and UM-UC-3, with G(1) cell cycle arrest and altered cyclin B1/D1 expression in RT-4, whereas Rb up-regulation occurred in UM-UC-3. Apoptosis occurred in both cell lines. Celecoxib induces G(1) cell cycle arrest in low- and high-grade bladder cancer by different pathways. This heterogeneous molecular response supports combination approaches to prevention and treatment. Written by: Reference: PubMed Abstract UroToday.com Bladder Cancer Section
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