Study on the mechanism of apoptosis induced by low-dose LBH 589 through PI3K/AKT pathway in epithelial ovarian cancer cells

ObjectiveTo investigate the effects of low-dose LBH589 on the apoptosis of epithelial ovarian cancer cells induced by PI3K/AKT pathway.

MethodsThe apoptosis and cycle of epithelial ovarian cancer cells(OVCAR-3 cells) in the experimental group with low-dose LBH589 inducing and control group without low-dose LBH589 inducing were detected using TUNEL and flow cytometry, respectively.The inhibition of low-dose LBH589 on epithelial overian cancer cell proliferation was detected using MTT assay, and the expression levels of PI3K, AKT p-PI3K and p-AKT in two groups were detected using Western blot ting.

ResultsThe cell apoptosis index in experimental group was significantly higher than that in control group(P < 0.01), the number of epithelial ovarian cancer cells in S-phase in experimental group was significantly lower than that in control group(P < 0.01).The inhibitory rates of epithelial ovarian cancer cells in experimental group at 12, 24, 36 and 48 h were(12.35±0.27)%, (21.24±0.33)%, (33.54±0.26)% and(41.23±0.52)%, respectively.The inhibition rate in control group was 0.In experimental group, the sensitivity of EOC cells to cisplatin significantly increased(P < 0.01), and the reversal coefficient was 3.26 times of control group.Compared with the control group, the expression levels of PI3K, AKT, p-PI3K and p-AKT in ovarian cancer cells were significantly inhibited in experimental group(P < 0.01).

ConclusionsThe low-dose LBH589 can increase the apoptosis of the epithelial ovarian cancer cells OVCAR-3, and may reverse the cisplatin resistance through the PI3K/AKT pathway.