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Anticancer Res. 2009 Oct;29(10):3769-75.

Cyclin-mediated G1 arrest by celecoxib differs in low-versus high-grade bladder cancer.

Author information

1
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. Gee@urology.wisc.edu

Abstract

BACKGROUND:

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.

MATERIALS AND METHODS:

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.

RESULTS:

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.

CONCLUSION:

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.

PMID:
19846907
PMCID:
PMC2955297
[Indexed for MEDLINE]
Free PMC Article

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