Effects Of Melatonin On Cell Proliferation,Cell Cycle And Apoptosis Of Leukemia Stem-like Cell KG1a Cell Lines

Objective: To investigate the effects of melatonin on the viability,proliferation,cell cycle distribution and apoptosis of KG1 a cells in vitro,and to preliminarily explore its possible anti-leukemia stem cell mechanism,so as to provide new drugs and therapeutic ideas for the therapy of acute myeloid leukemia.Methods: CCK8 assay was used to detect the KG1 a cell viability after treated with Melatonin.Edu staining was employed to evaluate the effect of Melatonin on the proliferation of KG1 a cells.The colony formation experiment was used to detect the effect of Melatonin on the self-renewal ability of human leukemia KG1 a cells.Flow cytometry was administrated to measure the effect of Melatonin on the cell cycle and apoptosis of KG1 a cells.The apoptosis change was further examined by TUNEL staining.Western blot was performed to access the effect of Melatonin on the activation of PARP and the protein expression levels of Bcl2 and Bax in KG1 a cells.Results: The results of CCK-8 assay showed that the cell viability was obviously decreased after treated with different concentration of Melatonin,the IC50 of 24 h and48h were(1.28±0.65)m M and(0.26±0.73)m M respectively.Edu assay showed that Melatonin could obviously inhibit the proliferation of KG1 a cells.The colony formation showed Melatonin could suppress the stemness of KG1 a cells.Flow cytometry revealed that Melatonin could arrest KG1 a cells in G1/S phase and induce apoptosis of KG1 a cells.TUNEL assay further confirmed that Melatonin could induce apoptosis of KG1 a cells.Western blot showed that Melatonin could induce PARP activation in KG1 a cells,increase the expression of pro-apoptotic protein Bax and decrease the expression of anti-apoptotic protein Bcl-2.Conclusion: Melatonin has a significant suppression effects on the growth of KG1 a cells in dose and time-dependent manners,and exerts its anti-leukemia effects by triggering apoptosis and cell cycle arrest.The potential mechanism may be associated with the up-regulation the protein levels of cleaved PARP and Bax,and downregulation protein levels the of Bcl-2,the potential anti-leukemia mechanism need further investigation.