[A study on the apoptosis of gastric carcinoma cells induced by arsenic trioxide combined with Ad-IkappaBalphaM].

2007 
Objective To study the activation of nuclear facter-κB(NF-κB)in gastric carcinoma SGC-7901 cells after treating with As_2O_3 and the enhancement of the therapeutic effect of As_2O_3 with recombinant adenovirus IκBαM.Methods Culture of gastric carcinoma SGC-7901 cells was carried out. The cells both uninfected and infected with Ad-IκBα but not treated with As_2O_3 were used as control. Electrophoretic mobility shift assay(EMSA)and immunohistochemistry were used to detect the activation of NF-κB in the cells after treatment of As_2O_3 and the combination with Ad-IκBαM.MTr,Hoechest staining and TUNEL were used to assay the change of apoptosis induced by As_2O_3 after infection with Ad-IκBαM. Results The results of EMSA and immunohistochemical method showed that after the treatment of As_2O_3 the cells showed high activity of NF-κB.Simultaneous infection with Ad-IκBαM can inhibit the activation of NF-κB;MTT method indicated that after the treatment of As_2O_3 infected with Ad-IκBαM apoptosis rate of the cells(59.2±2.5)% was higher than that of the cells treated with As_2O_3 and infected with Ad-IκBα but not treated with As_2O_3(47.5±2.3)% and these neither infected nor treated(40.0±1.2% ),P0.01. The result of Hoechest staining method indicated that,in the group of cells treated with As_2O_3 and infected with Ad-IκBαM,apoptosis rate is(27.7±2.6)%,which was higher than the that of the cells infected with Ad-IκBα(18.3±1.5)% but not treated with As_2O_3 and these neither infected nor treated(11.0±1.7 %), P0.05.Hoechest staining method was in accordance with TUNEL technique;it was shown that in the group of cells treated with As_2O_3 and infected with Ad-IκBαM,apoptosis rate was(31.1±2.5 )%,being still higher than that of cells infected with Ad-IκBα but not treated with As_2O_3(20.7±2.1)% and these neither infected nor treated(13.0±1.7)%,P0.01.Therefore,infection with Ad-IκBαM can significantly increase the apoptosis induced by As_2O_3.Conclusions Gastric carcinoma cells treated with As_2O_3 show activity of NF-κB.It is indicated that the activity of NF-κB may be the mechanism of the antagonism of gastric carcinoma cells against the apoptosis induced by As_2O_3.Infection with Ad-IκBαM can effectively inhibit the activation of NF-κB in gastric carcinoma cells and increase the cell apoptosis induced by As_2O_3.
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