Résumé
Objective The use of targeting therapy for the treatment of gastric glandular cancer has been a hot topic in recent years. This study aims to clarify that through what ways the histone deacetylase inhibitor MS-275 completes its selectively killing effect on gastric glandular cancer cell line SGC-7901. Methods SGC-7901 cells and GES-1 cells were respectively cultured for 24h, with(10-100) μmol/L concentrations of MS-275. (1) The survival rate of SGC-7901 cells, GES-1 cells and the normal cells were analyzed by WST-1; (2) The change of the mitochondrial membrane potential in SGC-7901 was estimated by flow cytometry;(3) The expression levels of p21, p27, p57, cyclinB1, cyclinD1 were determined by Western blot and PCR methods. Results (1) MS-275 could decrease the survival rate of SGC-7901 cells, the effect was significantly enhanced with the increasing of the concentration (P<0.05), but MS-275 showed no obvious effect on normal gastric mucosa epithelial cells GES-1; (2) MS-275 treatment could decreased the mitochondrial membrane potential of SGC-7901 cells (P<0.05); (3) MS-275 treatment could increase the relative contents of p21, p27, p57 genes and their protein and, at the same time, decrease the relative contents of CyclinB1 and CyclinD1 (P<0.05). Conclusion MS-275 treatment can selectively kill gastric glandular cancer cells SGC-7901 through several possible ways, such as inducing mitochondrial apoptosis and regulating the expression levels of cell cycle-related genes and proteins.