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Induction of Invasive Transitional Cell Bladder Carcinoma in Immune Intact Human MUC1 Transgenic Mice: A Model for Immunotherapy Development
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Cyclin-mediated G1 arrest by celecoxib differs in low-versus high-grade bladder cancer

Jason R Gee1, Corrie B Burmeister, Thomas C Havighurst

  • 1Department 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

Anticancer Research
|October 23, 2009
PubMed
Abstract

Insights

Celecoxib inhibits bladder cancer growth by causing cell cycle arrest. This non-steroidal anti-inflammatory drug (NSAID) affects low- and high-grade cancers through distinct molecular pathways, suggesting varied treatment strategies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Non-steroidal anti-inflammatory drugs (NSAIDs), including celecoxib, are explored for cancer prevention.
  • Investigating celecoxib's molecular effects in bladder cancer, independent of cyclooxygenase (COX)-2 levels.
  • Focus on urothelial carcinoma of the bladder.

Purpose of the Study:

  • To examine the molecular mechanisms of celecoxib in bladder cancer cells.
  • To understand celecoxib's effects on cell growth, cell cycle, and apoptosis.
  • To differentiate responses between low-grade and high-grade bladder cancer.

Main Methods:

  • Treatment of RT-4 (low-grade) and UM-UC-3 (high-grade) bladder cancer cells with varying concentrations of celecoxib.
  • Assessment of cell growth, cell cycle progression, and apoptosis using crystal violet elution and flow cytometry.
  • Western blot analysis to evaluate protein expression (COX-2, Rb, cyclin B1/D1, phospho-cyclin B1/D1).

Main Results:

  • Celecoxib demonstrated growth inhibition in both RT-4 and UM-UC-3 cell lines.
  • RT-4 cells exhibited G(1) cell cycle arrest with altered cyclin B1/D1 expression.
  • UM-UC-3 cells showed G(1) cell cycle arrest with Rb up-regulation; apoptosis was observed in both cell types.

Conclusions:

  • Celecoxib induces G(1) cell cycle arrest in bladder cancer cells via distinct molecular pathways.
  • The differential response highlights the heterogeneity of bladder cancer.
  • Findings support the potential for combination therapies in bladder cancer prevention and treatment.

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