Expression And Signification Of PI3k、Akt、p-Akt、Bad、p-Bad In Radiosensitivity Induced By Aresenic Trioxide In Human Esophageal Carcinoma

Background Esophageal cancer is one of the common malignant tumor, radiation therapy is one of the main treatment in advanced Esophageal cancer.But there are some vi-tal organs around the esophagus such as the spinal cord, lung,heart and so on.So high target dose can not be reached which limits the efficacy of radotherapy in esophageal cancer. So r-adiosensitization seems to be a necessary supporting measure to impove the efficacy of ra-dotherapy. Our team earlier study shows that As2O3can improve radiosensitivity in human Esophageal Carcinoma Cell EC-1line, But the mechanism remains unclear.Objective The aim of this study was to explore mechanism radiosensitivity induc-ed by aresenic trioxide in human Esophageal Carcinoma Cell line EC-1, which would pro-vide a theoretical basis for esophageal cancer treated with combined arsenic trioxide and r-adiation therapyMethods1.The experiments is divided into four groups, respectively blank control group (C), radiation therapy group(R),As203group,As203and R group (Co-treat),The Hu-man Esophageal Carcinoma Cell Line EC-1was treated individually with radiation therapy (2Gy)、As2O3(3μmol/L)、As2O3(3μmol/L) and radiation therapy(2Gy)(C o-treat),2. The expression of the PI3k、Ak、p-Akt and p-Bad of the PI3k/Akt signali-ng pathway components was determined by Western blotting.Results1. Compared with control group, the expression level of p-Akt declined in EC- 1Cell treated with R alone, As2O3alone or Co-treat(0.41±0.01;0.37±0.01;0.27±0.04V.S0.49±0.05,P<0.01).The expression of p-Akt decreased remarkablely in EC-1Cell treated with Co-treat compared with R alone, As2O3alone (0.27±0.04V.S0.41±0.01;0.37±0.01P<0.01),it had statistical significance.2. Compared with control group, the expression level of p-Bad declined in EC-lCell treated with R alone, As2O3alone or Co-treat (1.16±0.02;1.07±0.03;0.92±0.04V.S1.26±0.05,P<0.01). The expression of p-Bad decreased remarkablely in EC-1C-ell treated with Co-treat compared with R alone、As2O3alone (0.92±0.04V.S1.16±0.02;1.07±0.03,P<0.01),it had statistical significance.3. Compared with control group,the expression level of PI3k had no obvious dif-ference in EC-1Cell treated with R alone,As2O3alone or Co-treat (3.47±0.31;3.47±0.26;3.41±0.1SV.S3.51±0.22,P>0.05).Compared with R or As2O3alone,the expression of PI3k had no obvious difference in EC-1Cell treated with Co-treat (3.41±0.18V.S3.47±0.31;3.47±0.26,.P>0.05), it had no statistical significance.4. Compared with control group,the expression level of Akt had no obvious diffe rence in EC-1Cell treated with R alone, As2O3alone or Co-treat (3.52±0.11;3.57±0.22;3.50±0.26V.S3.61±0.13,.P>0.05).Compared with R or As2O3alone,the expression of Akt had no obvious difference in EC-1Cell treated with Co-treat (3.50±0.26V.S3.52±0.11;3.57±0.22,P>0.05), it had no statistical significance.5. Compared with control group,the expression level of Bad had no obvious diff-erence in EC-1Cell treated with R alone, As2O3alone or Co-treat (1.81±0.03;1.79±0.03;1.80±0.06V.S1.82±0.08,P>0.05). Compared with R or As2O3alone,the expression of Bad had no obvious difference in EC-1Cell treated with Co-treat (1.80±0.06V.S1.81±0.03;1.79±0.03,P>0.05), it had no statistical significance.ConclusionsAresenic Trioxide can improve radiotherapy sensitization probably through down-regulating expression of p-Akt and p-Bad.PI3K/Akt signaling pathways is possible o- ne of the mechanism radiotherapy sensitization induced by As2O3in Human Esoph-ageal Carcinoma Cell Line EC-1.