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Celecoxib inhibits STAT3 phosphorylation and suppresses cell migration and colony forming ability in rhabdomyosarcoma

Suzanne Reed1, Huameng Li, Chenglong Li

  • 1Center for Childhood Cancer, The Research Institute at Nationwide Children's Hospital, The Ohio State University, College of Medicine, Columbus, OH 43205, USA.

Biochemical and Biophysical Research Communications
|March 15, 2011
PubMed

Insights

Celecoxib effectively inhibits rhabdomyosarcoma cell viability and spread by targeting the STAT3 pathway. This finding suggests celecoxib as a potential therapy for aggressive or metastatic rhabdomyosarcoma.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Rhabdomyosarcoma (RMS) is a prevalent pediatric soft tissue sarcoma with poor outcomes for diffuse disease.
  • The signal transducer and activator of transcription 3 (STAT3) pathway is constitutively active in RMS, presenting a potential therapeutic target.
  • Targeting STAT3 signaling may induce tumor cell death in rhabdomyosarcoma.

Purpose of the Study:

  • To investigate the potential of celecoxib, a known cyclooxygenase-2 (COX-2) inhibitor, to target the STAT3 pathway in rhabdomyosarcoma.
  • To evaluate the effects of celecoxib on STAT3 phosphorylation, cell viability, and downstream gene expression in human RMS cells.
  • To assess celecoxib's impact on RMS cell colony formation and migration.

Main Methods:

  • Computer modeling to predict celecoxib binding to the STAT3 SH2 domain.
  • In vitro experiments using human rhabdomyosarcoma cells to assess celecoxib's effects on IL-6-induced STAT3 phosphorylation and cell viability.
  • Analysis of downstream STAT3 target gene expression (BCL-2, survivin, cyclin D1) following celecoxib treatment.
  • Colony formation and cell migration assays were performed to evaluate functional changes.

Main Results:

  • Celecoxib was shown to inhibit both IL-6-induced and persistent STAT3 phosphorylation in human RMS cells.
  • Celecoxib significantly reduced RMS cell viability.
  • Downstream STAT3 target genes, including BCL-2, survivin, and cyclin D1, were downregulated by celecoxib.
  • Celecoxib inhibited colony formation and cell migration in RMS cells.

Conclusions:

  • Celecoxib demonstrates efficacy against rhabdomyosarcoma cells through inhibition of the STAT3 pathway, independent of its COX-2 inhibitory activity.
  • The observed inhibition of cell viability, colony formation, and migration suggests celecoxib holds therapeutic potential for RMS.
  • Celecoxib may be a valuable agent for treating advanced or metastatic rhabdomyosarcoma, where current outcomes are limited.

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