Although anticancer therapies for leukemia have been well-established, it does not change the fact that not only leukemia has significantly caused a high number of deaths but also projected to further increase in the future. Previous studies have reported that melatonin exerts numerous anticancer effects on different cancers, including leukemia. However, the underlying mechanisms that cause melatonin’s effect on leukemic cells remain not fully elucidated. In this study, the role of mitophagy in melatonin-treated leukemic cells was investigated. The JURKAT cell line was used as a T-cell acute lymphoblastic leukemia (T-ALL) cell model and treated with melatonin. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay was used to investigate cell viability. The presence of autophagy was determined via acridine orange staining. Western blot analysis was implemented to quantify the expressions of proteins. Observations of cell death and autophagic vacuoles induced by melatonin were according to a dose-dependent manner. The study results showed elevated levels of SQSTM1/p62, Optineurin, NDP52, BNIP3 and BNIP3L/Nix proteins compared to the control group, indicating their increased expression in this pathway. In conclusion, melatonin poses the potential to be used as an anticancer therapeutic agent for T-ALL.
Key words: Melatonin, mitophagy, anti-cancer, Jurkat cells, autophagy, Leukemia
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