Abstract
Acute myeloid leukemia (AML) is a life-threatening aggressive malignancy of the bone marrow and has posed a great challenge to the clinic, due to a lack of fully understanding of the molecular mechanism. Histone deacetylase 1 (HDAC1) has been reported to be a therapeutic target for treating AML. Naringenin (Nar) may act as an anti-leukemic agent and suppress the expression of HDACs. However, the potential underlying mechanism of Nar in suppressing the activity of HDAC1 remains unclear. Here, we found that Nar induced the apoptosis, decreased the expression of lncRNA XIST and HDAC1, and increased the expression of microRNA-34a in HL60 cells. Sh-XIST transfection could induce cell apoptosis. On the contrary, the forced expression of XIST might reverse the biological actions of Nar. XIST could sponge miR-34a, which targeted to degrade HDAC1. The forced expression of HDAC1 could effectively reverse the effects of Nar. Thus, Nar can induce cell apoptosis by mediating the expression of lncRNA XIST/miR-34a/HDAC1 signaling in HL60 cells.