The Molecular Mechanisms Of Celecoxib In The Inhibition Of Nasopharyngeal Carcinoma Cells Proliferation

Objective:To investigate the effect of celecoxib on proliferation, apoptosis and cell cycle distribution in nasopharyngeal carcinoma cells.Methods:MTT assay was performed to evaluate the effect of different drug concentrations (5,10,25,50,75μmol/L) of celecoxib on proliferation of nasopharyngeal carcinoma cells at48h. The flow cytometry was used to detect the apoptosis and cell cycle distribution in HNE1and CNE1-LMP1cells after celecoxib treatment with different doses (10,25,50or75μmol/L) for48h.Results:MTT results showed that celecoxib could inhibit nasopharyngeal carcinoma cells proliferation in concentration-dependent manner. Flow cytometry showed that (25,50μmol/L) celecoxib could induce HNE1apoptosis and G0/G1phase cell cycle arrest,(50,75μmol/L) of celecoxib could induce CNE1-LMP1cells apoptosis and (25,50,75μmol/L) celecoxib could induce CNE1-LMP1cells G0/G1phase cell cycle arrest.Conclusion:Celecoxib can inhibit nasopharyngeal HNE1and CNE1-LMP1cell proliferation, induce tumor cell apoptosis and cell cycle arrest in G0/G1phase. Objective:To investigate the effect of celecoxib on IL-6/STAT3signal pathway in nasopharyngeal carcinoma cells.Methods:Western Blot was performed to evaluate the STAT3, pSTAT3, Survivin, Mcl-1, Bcl-2and Cyclin D1protein expression after celecoxib treatment with different concentrations of celecoxib (0,10,25,50or75μmol/L) for48h in nasopharyngeal carcinoma HNE1and CNE1-LMPl cells. Western Blot was also used to detect whether celecoxib could inhibit exogenous IL-6-induced STAT3phosphorylation.Results:Phosphorylation STAT3y705(pSTAT3y705) expression was significantly decreased after celecoxib treatment with10,25,50μmol/L in HNE1cells, accordingly, Survivin, Mcl-1, Bcl-2and Cyclin D1protein expression were also decreased. In addition, the phosphorylation of STAT3y705(pSTAT3y705) expression was significantly down-regulated after celecoxib treatment with25,50,75μmol/L in CNE1-LMP1cells, meanwhile, Survivin, Mcl-1, Bcl-2and Cyclin D1protein expression were also down-regulated. Celecoxib can also inhibit exogenous IL-6-induced STAT3phosphorylation.Conclusion:Celecoxib can inhibit phosphorylation of STAT3y705in nasopharyngeal carcinoma cells and down-regulate Survivin, Mcl-1, Bcl-2and Cyclin Dl protein expression. Objective:To explore the effect of celecoxib on AKT phosphorylation in nasopharyngeal carcinoma cells.Methods:Western Blot was also used to detect AKT phosphorylation protein expression after celecoxib treatment with different concentrations of celecoxib (25,50and75μmol/L) for48h in nasopharyngeal carcinoma HNE1、CHNE1-LMP1and HONE1cells.Results:Western Blot results showed that celecoxib can inhibit AKT phosphorylation in nasopharyngeal carcinoma HNE1、CNE1-LMP1and HONE1cells.Conclusion: Celecoxib can inhibit AKT phosphorylation of nasopharyngeal carcinoma cells.