Study on the Mitochondrial Autophagy Pathway of Apoptosis Induced by Deferoxamine in the Leukemia Cell Line HL-60

Background: Acute leukemia isoneof the most common malignant tumors in children, andit is mainly treated with a combination of chemotherapy and hematopoietic stem cell transplantation. At present, there are many problems with these treatments, such as significant adverse reactions, quick acquisition of drug resistance, and early recurrence. There are no reports on the treatment of leukemia by the mitophagy pathway. Therefore, exploring new ways to treat leukemia has become an urgent task for the effective treatment of leukemia. Objectives: This study aimed to explore the role of the mitochondrial autophagy-mediated apoptosis pathway in deferoxamine (DFO)-induced apoptosis of HL-60 cells and provide an additional experimental basis for the clinical treatment of leukemia with DFO. Methods: Through cell viability detection, Hoechst 33342 staining, and annexin V-APC/7-AAD double staining, we proved that DFO could induce apoptosis in HL-60 cells. Through the determination of intracellular reactive oxygen species (ROS) levels, western blot detection of the mitochondria-related proteins, heat shock protein 60 (HSP60), nip-like protein X (NIX), translocase of inner mitochondrial membrane 23 (TIMM23), translocase of the outer mitochondrial membrane member 20 (TOMM20), quantitative realtime polymerase chain reaction (PCR) detection of the RNA levels of NIX, microtubule-associated protein 1 light chain 3 (LC3), and TIMM23, we demonstrated that DFO induced mitochondrial autophagy in HL-60 cells. Results: DFO induced apoptosis and mitochondrial autophagy in HL-60 cells. Conclusions: This study demonstrated that DFO further induced apoptosis by inducing autophagy in leukemic cells, which provides another experimental basis for the clinical treatment of leukemia with DFO.