title: Anticancer effects of celecoxib through inhibiton of STAT3 phosphorylation and AKT phosphorylation in nasopharyngeal carcinoma cell lines.
abstract: Previously, we showed that treatment with celecoxib obviously inhibited proliferation of nasopharyngeal carcinoma (NPC) cell lines in a dose-dependent manner. However, the underlying molecular mechanisms of its anticancer effect on NPC have not been fully clarified. The present in vitro study was performed to investigate the mechanisms involved in the anticancer effect of celecoxib in NPC. NPC cell line HONE1 was treated with celecoxib at varying concentrations. The antiproliferation effect of celecoxib on the HONE1 cell line was assessed with methyl thiazolyl tetrazolium (MTT) assay. Western blot analysis of signal transducer and activator of transcription 3 (STAT3), phosphorylated STAT3(Y705) (pSTAT3(Y705)), Survivin, Mcl-1, Bcl-2 and Cyclin D1 was carried out at various concentration of celecoxib for 48 h in HONE1 cell line. Western blot analysis of Protein Kinase B (AKT), phosphorylated AKT (pAKT) was performed at increasing doses of celecoxib for 48 h in HNE1, CNE1-LMP1 and HONE1 cells. The results showed that celecoxib inhibited proliferation of HONE1 cell line in a dose-dependent manner. Celecoxib inhibited the activation of STAT3 phosphorylation in HONE1 cells and the downstream genes of STAT3 (Survivin, Mcl-1, Bcl-2 and Cyclin D1) were downregulated after treatment with celecoxib. Furthermore, celecoxib could inhibit AKT phosphorylation in HNE1, CNE1-LMP1 and HONE1 cell lines. These data suggested that celecoxib was a promising agent for the chemoprevention and treatment of NPC.
authors.forename: Dong-Bo
authors.initials: DB
authors.lastname: Liu
authors.forename: Guo-Xian
authors.initials: GX
authors.lastname: Long
authors.forename: Qi
authors.initials: Q
authors.lastname: Mei
authors.forename: Jun-Feng
authors.initials: JF
authors.lastname: Wang
authors.forename: Guang-Yuan
authors.initials: GY
authors.lastname: Hu
authors.forename: Lei
authors.initials: L
authors.lastname: Gan
authors.forename: Wen-Wen
authors.initials: WW
authors.lastname: Li
authors.forename: Wei
authors.initials: W
authors.lastname: Sun
authors.forename: Shun-Fang
authors.initials: SF
authors.lastname: Liu
authors.forename: Ji-Zong
authors.initials: JZ
authors.lastname: Jiang
authors.forename: Guo-Qing
authors.initials: GQ
authors.lastname: Hu
mesh_terms: D000970:Antineoplastic Agents; D015153:Blotting, Western; D000068579:Celecoxib; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D004396:Coloring Agents; D052246:Cyclooxygenase 2 Inhibitors / Q000494:pharmacology*; D006801:Humans; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D011720:Pyrazoles / Q000494:pharmacology*; D050796:STAT3 Transcription Factor / Q000378:metabolism*; D013449:Sulfonamides / Q000494:pharmacology*; D013778:Tetrazolium Salts; D013844:Thiazoles
chemical_list: D000970:Antineoplastic Agents; D004396:Coloring Agents; D052246:Cyclooxygenase 2 Inhibitors; D011720:Pyrazoles; D050796:STAT3 Transcription Factor; D013449:Sulfonamides; D013778:Tetrazolium Salts; D013844:Thiazoles; D051057:Proto-Oncogene Proteins c-akt; C022616:thiazolyl blue; D000068579:Celecoxib