Curcumin Inhibits the Growth and Induces Apoptosis of Human Endometrial Cancer Cells.

The objective of this study was to analyze the mechanism of curcumin inhibiting the growth and inducing apoptosis of human endometrial carcinoma cell line. Human endometrial carcinoma cell line was cultured in vitro and all cells were divided into control group, curcumin low, medium and high treatment group, the concentrations were 5 mg/l, 10 mg/l and 20 mg/l, respectively. Compared with the non-medicated control group, the proliferation of human endometrial carcinoma cell treated with curcumin at different concentrations for 24, 48 and 72 h was significantly inhibited and with the increase of drug concentration, the inhibition rate was significantly increased in a dose-dependent manner (p<0.05). After treatment of human endometrial carcinoma cell with curcumin 5 mg/l, 10 mg/l and 20 mg/l, the ratio of growth 0/growth 1 was significantly lower than that of the control group, the ratio of growth 2/mitosis phase was significantly higher than that of the control group and the ratio of growth 2/mitosis phase was gradually increased with the increase of drug concentration, which was dose-dependent (p<0.05). After treatment of human endometrial carcinoma cells with curcumin 5 mg/l, 10 mg/l and 20 mg/l, the apoptosis rate gradually increased and with the increase of drug concentration, the apoptosis rate increased sequentially (p<0.05). After treatment of human endometrial carcinoma cell with curcumin 5 mg/l, 10 mg/l and 20 mg/l, compared with the control group, the protein level of apoptosis factor Livin was significantly decreased and the protein level of caspase-3 was significantly increased in each group (p<0.05). The levels of Livin protein and caspase-3 protein were dose-dependent with curcumin concentration. It was concluded that curcumin has obvious inhibitory effect on human endometrial cancer cells and can induce cell cycle arrest, promote apoptosis, which is concentration dependent. The related reason may be through inhibiting Livin protein expression and increasing caspase-3 protein level. [ABSTRACT FROM AUTHOR]