Propranolol-induced apoptosis via the AKT signaling pathway in epithelial ovarian cancer

Abstract Objective: This study aims to explore whether the effect of propranolol on the viability and apoptosis of ovarian cancer cells is mediated by inhibiting AKT signaling pathway. Methods: SKOV-3 ovarian cancer cell was treated with 0, 25, 50, 100, 200 and 400μM propranolol hydrochloride for 0, 24, 48, and 72 h, and then the cell viability was detected by CCK-8. After treating SKOV-3 cells with 0, 50, 100, and 200μM propranolol for 24h, Q-PCR detected the mRNA levels of BCL-2, BAX, and AKT. Western blotwas employed to detect the protein expression of caspase-3 and AKT. The activator N-oleoylglycine and the inhibitor A2D5363 were combined with propranolol to treat SKOV-3 cells for 24h. Western blot detected the protein expression of AKT and CCK-8 method was used to detect cell proliferation. Results: Propranolol inhibited the proliferation of SKOV-3 cells in a concentration- and time-dependent manner. In addition, propranolol promoted the expressions of BAX and caspase-3 and inhibited BCL-2 and AKT. Propranolol combined with AKT inhibitor A2D5363 enhanced the propranolol anti-ovarian cancer effect and the combined with AKT activator N-Oleoylglycine reduced the anti-ovarian cancer effect of propranolol. Conclusions: Propranolol-induced apoptosis of ovarian cancer is mediated by inhibiting the AKT signaling pathway.