Mechanism of β-catenin/Akt signaling pathway in apoptosis of gastric cancer cells induced by selenite sodium / 中国生化药物杂志

ABSTRACT

Objective To explore the mechanism of β-catenin/Akt signaling pathway in the apoptosis of gastric cancer cells induced by selenite sodium.Methods Gastric cancer cell line SGC-7901 was cultured, and 0 mol/L, 5 mol/L, 10 mol/L and 20 mol/L selenite sodium treated cells; flow cytometry was used to detect the cell apoptosis rate after 24 h;10 mol/L sodium selenite treated cells, flow cytometry was used to detect the cell cycle changes after 24 h;10 mol/L sodium selenite treated cells,protein expression ofβ-catenin,cyclin D1 and protein kinase B ( Akt) activity were detected by Western blot after 0,6,12,24 h.Results Cells apoptosis rate was significantly higher than 0 mol/L after cells was treated by 5 mol/L, 10 mol/L and 20 mol/L sodium selenite, due to cells apoptosis rate was higher by 10 mol/L sodium selenite treated than 5 mol/L and 20 mol/L, 10 mol/L sodium selenite treated cells for follow-up study;gastric cancer cells was treated by 10 mol/L sodium selenite for 24 h, compared with the control group, G0/G1 phase cells decreased, cells in S phase and G2/M phase significantly increased(P<0.05);gastric cancer cells was treated by 10 mol/L sodium selenite for 0 h, 6 h, 12 h and 24 h,protein expression of β-catenin and cyclin D1 and Survivin in 6 h, 12 h and 24 h was significantly lower than that in 0 hour (P<0.01),and with the extension of time, protein expression gradually decreased;gastric cancer cells was treated by 10 mol/L sodium selenite could significantly decrease the phosphorylation of p-Akt in 6,12,24 h, while there was no significant difference of Akt among difference time points( P <0.01).Conclusion Sodium selenite could induce apoptosis of gastric cancer cells, and the cells were arrested in S phase.The mechanism may be associated with beta-catenin/Akt signaling pathway.