Abstract

To explore the effect of esomeprazole on the biological characteristics of hepatoma cells by regulating protein kinase B/forkhead box O3 pathway. Hepatoma cell lines were cultured and subcultured and divided into model group, low dose group and high dose group. The changes of proliferation, colony formation and apoptosis of hepatoma cells in each group and the expression levels of proliferation, apoptosis related proteins and protein kinase B/forkhead box O3 pathway related proteins were detected. Esomeprazole inhibited tumor cells in a time and dose-dependent manner and the difference was statistically significant (p<0.05). With the increase of drug dose, the number of liver cancer cell colony formation decreased gradually and the difference was statistically significant (p<0.05). Esomeprazole induced apoptosis of tumor cells in a time and dose-dependent manner and the difference was statistically significant (p<0.05). Compared with the model group, the expression levels of cyclin-dependent kinase 1, cyclin-dependent kinase 2, cyclin A2 and cyclin E2 decreased with the increase of esomeprazole dose (p<0.05). Compared with the model group, the level of apoptotic protein procaspase-9 in high and low dose groups decreased significantly, while the level of cleaved caspase-9 increased in a dose-dependent manner (p<0.05). The level of protein kinase B in high dose group was lower than that in model group and low dose group, while the level of forkhead box O3 protein increased; the difference was statistically significant (p<0.05). Esomeprazole can affect the biological characteristics of tumor cells such as proliferation and apoptosis by activating protein kinase B/forkhead box O3 pathway, which provides a new method for the treatment of liver cancer.