Dimethyl-celecoxib (DMC), a derivative of celecoxib that lacks cyclooxygenase-2-inhibitory function, potently mimics the anti-tumor effects of celecoxib on Burkitt's lymphoma in vitro and in vivo

Cancer Biol Ther. 2005 May;4(5):571-82. doi: 10.4161/cbt.4.5.1699. Epub 2005 May 5.


The nonsteroidal anti-inflammatory drug (NSAID) celecoxib is a selective cyclooxygenase-2 (COX-2) inhibitor that has shown some promising results as an anti-cancer drug. However, the question arose as to whether or not its COX-2-inhibitory function is required for its anti-tumorigenic properties. We therefore employed dimethyl-celecoxib (DMC), which is a close structural analog of celecoxib that lacks COX-2-inhibitory function, to investigate this question. By performing a combination of in vitro and in vivo studies with Burkitt's lymphoma cells, we found that DMC potently mimics all of the anti-proliferative and anti-tumorigenic effects of celecoxib. In cell culture, DMC effectively inhibits cell proliferation through the down-regulation of cyclins A and B and the ensuing loss of cyclin-dependent kinase activity. This effect appears to take place in vivo as well and results in significantly (p<.002) reduced tumor growth in experimental animals. Thus, our results demonstrate that the anti-proliferative and anti-tumorigenic properties of celecoxib and DMC are indistinguishable, at least in Burkitt's lymphoma cells, and therefore, that the COX-2-inhibitory function is not required for these effects.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology
  • Burkitt Lymphoma / drug therapy*
  • Burkitt Lymphoma / metabolism
  • Burkitt Lymphoma / pathology
  • Celecoxib
  • Cell Cycle Proteins / analysis
  • Cell Cycle Proteins / metabolism
  • Cell Line, Tumor
  • Cell Survival / drug effects
  • Cyclooxygenase Inhibitors / chemical synthesis
  • Cyclooxygenase Inhibitors / chemistry
  • Cyclooxygenase Inhibitors / pharmacology*
  • Dinoprostone / analysis
  • Dinoprostone / metabolism
  • Dose-Response Relationship, Drug
  • Immunohistochemistry
  • In Vitro Techniques
  • Male
  • Mice
  • Mice, Nude
  • Molecular Structure
  • Neoplasm Transplantation
  • Pyrazoles / chemical synthesis
  • Pyrazoles / chemistry
  • Pyrazoles / pharmacology*
  • Sulfonamides / chemical synthesis
  • Sulfonamides / chemistry
  • Sulfonamides / pharmacology*
  • Transplantation, Heterologous
  • Xenograft Model Antitumor Assays


  • 2,5-dimethylcelecoxib
  • Antineoplastic Agents
  • Cell Cycle Proteins
  • Cyclooxygenase Inhibitors
  • Pyrazoles
  • Sulfonamides
  • Celecoxib
  • Dinoprostone