Cdc20 protects cells from Ara-c-induced apoptosis in AML via targeting  autophagy

Abstract ObjectiveThis study aims to explore the role and mechanism of Cdc20 on Ara-c chemosensitivity of AML cells.MethodsEvaluation experiments of effects of Cdc20 on Ara-c chemosensitivity were performed with AML cell transfected with constructs overexpressing Cdc20 or AML cell transfected with Cdc20 shRNA through observing cell viability, apoptosis rate,expression of apoptosis protein.The level of autophagy was assessed by transmission electron microscopy and western blotting.ResultsAfter exposure to Ara-c, Cdc20 expression is down-regulated. Intracellular Cdc20 expression inhibited Ara-c-induced apoptosis as shown by increasing cell viability and decreasing expression of cleaved caspase3.The expression of LC3B was mediated by Cdc20 expression,which further inhibits autophagy. Moreover, Cdc20 mediated LC3B-decreasing promotes the expression of P-Akt and P-ERK and inhibits ROS generation.ConclusionIt was determined that Cdc20 promoted the degradation of LC3B, thereby inhibiting autophagy and decreasing Ara-c-induced apoptosis in AML cells.