Non-steroidal anti-inflammatory drugs to potentiate chemotherapy effects: from lab to clinic

Crit Rev Oncol Hematol. 2007 Jan;61(1):52-69. doi: 10.1016/j.critrevonc.2006.07.001. Epub 2006 Sep 1.


Most solid tumors express the cyclooxygenase-2 (COX-2) protein, a target of NSAIDs. COX-2 overexpression in tumorsis considered a predictor of more advanced stage disease and of worse prognosis in a number of studies investigating solid malignancies. Therefore, NSAIDs are evaluated as anti-cancer drugs. NSAIDs inhibit proliferation, invasiveness of tumors, and angiogenesis and overcome apoptosis resistance in a COX-2 dependent and independent manner. This review will focus on the rationale behind NSAIDs, including selective COX-2 inhibitors, in combination with conventional chemotherapeutic drugs or novel molecular targeted drugs. Studies investigating anti-cancer effects of NSAIDs on cell lines and xenograft models have shown modulation of the Akt, NF-kappaB, tyrosine kinase and the death receptor-mediated apoptosis pathways. COX-2 expression in tumors is not yet used as biomarker in the clinic. Despite the increased risk on cardiovascular toxicity induced by selective COX-2 inhibitors, several ongoing clinical trials are still investigating the therapeutic benefits of NSAIDs in oncology. The anti-tumor effects in these trials balanced with the side effects data will define the precise role of selective COX-2 inhibitors in the treatment of cancer patients.

Publication types

  • Review

MeSH terms

  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology*
  • Antineoplastic Agents / pharmacology*
  • Cyclooxygenase 2 Inhibitors
  • Drug Synergism
  • Drug Therapy, Combination
  • Humans


  • Anti-Inflammatory Agents, Non-Steroidal
  • Antineoplastic Agents
  • Cyclooxygenase 2 Inhibitors