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Related Experiment Videos

Celecoxib toxicity is cell cycle phase specific.

Jonathan M Bock1, Sarita G Menon, Lori L Sinclair

  • 1Department of Otolaryngology-Head and Neck Surgery, University of Iowa Hospital and Clinics, 200 Hawkins Drive, Iowa City, IA 52242, USA.

Cancer Research
|April 19, 2007
PubMed
Summary
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Celecoxib halts head and neck cancer cell growth by inducing p21(waf1/cip1) and G(1) arrest, leading to S phase toxicity. This involves decreased cyclin D1 and E2F-1, impacting cell proliferation.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Celecoxib demonstrates anti-cancer properties by inhibiting proliferation and inducing apoptosis in human tumors.
  • The precise molecular mechanisms underlying celecoxib's effects on cancer cells remain incompletely understood.

Purpose of the Study:

  • To investigate celecoxib's toxicity in head and neck squamous cell carcinomas (HNSCC).
  • To explore the relationship between celecoxib-induced cell cycle inhibition and toxicity in HNSCC.

Main Methods:

  • In vitro and in vivo proliferation assays using UM-SCC-1 and UM-SCC-17B cell lines.
  • Cell cycle analysis, Western blotting for p21(waf1/cip1), cyclin D1, Rb, and E2F-1.
  • Luciferase reporter assays to assess E2F transactivating activity.

Related Experiment Videos

  • Cell cycle phase-specific cytometric sorting to determine toxicity.

    • Main Results:

    • Celecoxib inhibited HNSCC proliferation and induced G(1) phase cell cycle arrest and apoptosis.
    • Celecoxib transcriptionally induced p21(waf1/cip1) independently of p53, decreasing cyclin D1 and Rb phosphorylation, and inhibiting nuclear E2F-1.
    • Clonogenic toxicity was preferentially induced in S phase cells, with lower p21(waf1/cip1) and cyclin D1 levels observed in this phase.

    Conclusions:

    • Celecoxib exhibits significant antiproliferative activity in head and neck cancer via p21(waf1/cip1) induction and G(1) arrest.
    • The study identifies S phase-specific toxicity, potentially mediated by profound inhibition of nuclear E2F function.