title: Effects of celecoxib treatment over the AKT pathway in head and neck squamous cell carcinoma.
abstract: BACKGROUND
  Celecoxib, a non-steroidal anti-inflammatory drug that selectively inhibits cyclooxygenase-2 (COX-2), has shown an important anticarcinogenic effect for the treatment of squamous cell carcinoma. The use of COX-2 inhibitors has effectively inhibited the growth of Head and Neck Squamous Cell Carcinoma (HNSCC) cell lines, while a recent phase 1 trial demonstrated good response rate of cancer cells to this drug with minimal toxicity. Possible targets of celecoxib include proteins involved in cell proliferation and apoptosis control. Additionally, celecoxib antitumoral activity has been linked with a COX-2-independent event.
  
  
  METHODS
  To better understand which cellular mechanisms are targeted by celecoxib, its effects upon the Akt signaling pathway using two different HNSCC cell lines were analyzed through cell viability assay, immunofluorescence, and Western blotting.
  
  
  RESULTS
  The results showed decreased levels of Cyclin D1 and pAkt protein expression in vitro. The number of viable cells was also diminished after celecoxib treatment.
  
  
  CONCLUSIONS
  As Akt pathway seems to be a valuable target for the HNSCC therapy, the results presented herein confirm that celecoxib can be considered as an alternative adjuvant drug for HNSCC treatment.
authors.affiliation: Department of Oral Pathology, School of Dentistry, University of São Paulo, São Paulo, Brazil; Department of Pathology and Oral Diagnosis, School of Dentistry, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
authors.forename: Aline Corrêa
authors.initials: AC
authors.lastname: Abrahão
authors.forename: Fernanda Salgueiredo
authors.initials: FS
authors.lastname: Giudice
authors.forename: Felipe Fornias
authors.initials: FF
authors.lastname: Sperandio
authors.forename: Décio dos Santos
authors.initials: Ddos S
authors.lastname: Pinto Junior
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D015153:Blotting, Western; D002294:Carcinoma, Squamous Cell / Q000473:pathology*; D000068579:Celecoxib; D018929:Cell Culture Techniques; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D019938:Cyclin D1 / Q000187:drug effects; D052246:Cyclooxygenase 2 Inhibitors / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D005455:Fluorescent Antibody Technique; D006258:Head and Neck Neoplasms / Q000473:pathology*; D006801:Humans; D019869:Phosphatidylinositol 3-Kinases / Q000187:drug effects; D051057:Proto-Oncogene Proteins c-akt / Q000187:drug effects*; D011720:Pyrazoles / Q000494:pharmacology*; D015398:Signal Transduction / Q000187:drug effects*; D013449:Sulfonamides / Q000494:pharmacology*
chemical_list: D000970:Antineoplastic Agents; C530104:CCND1 protein, human; D052246:Cyclooxygenase 2 Inhibitors; D011720:Pyrazoles; D013449:Sulfonamides; D019938:Cyclin D1; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D000068579:Celecoxib
keywords: Akt signaling pathway; cyclooxygenase-2 selective inhibitor; head and neck squamous cell carcinoma