AIM: To investigate the role of Forkhead box M 1 ( FoxM1 ) and B-cell leukemia/lymphoma-2 (Bcl-2) in the pathogenesis of acute myeloid leukemia (AML).METHODS:RT-qPCR and immunofluorescence analysis were used to determine the expression of FoxM 1 at mRNA and protein levels in AML-de novo patients, AML-complete re-mission (CR) patients, AML-refractoriness and relapse (RR) patients and healthy controls.HL60 cells and K562 cells were transfected with FoxM1 siRNA.The cell proliferation was detected by cell proliferation assay and colony formation as-say on soft agar, and the cell apoptosis was determined by flow cytometry .The expression of FoxM1 and Bcl-2 at mRNA and protein levels was detected by RT-qPCR and Western blotting .The activity of bcl-2 promoter was examined by lucifer-ase reporter assay with FoxM1 targetting.RESULTS:FoxM1 expression level in the AML-de novo patients was significant-ly higher than that in the healthy controls .As compared with the AML-de novo patients, FoxM1 expression in the AML-CR patients was reduced , and the FoxM1 expression level was the highest in the AML-RR patients .FoxM1 expression was in-hibited in the HL60 cells and K562 cells transfected with FoxM1 siRNA.Transfection with FoxM1 siRNA in the HL60 cells and K562 cells inhibited the proliferation as compared with NC siRNA transfection , and impaired the colony formation abili-ty.On the contrary , transfection with FoxM1 siRNA promoted the cell apoptosis .FoxM1 regulated bcl-2 expression posi-tively.CONCLUSION:FoxM1 promotes the development of AML by regulating bcl-2 expression.Silencing of FoxM1 ex-pression suppresses cell proliferation and promotes cell apoptosis .FoxM1 is a potential target for AML treatment .

AIM:To study whether inhibition of forkhead box protein M1(FoxM1) sensitizes leukemia K562 cells to homoharringtonine ( HHT ) .METHODS: K562 cells were incubated with HHT at different concentrations ( 0μmol/L, 0.015 μmol/L, 0.030μmol/L and 0.045μmol/L) for different time (0 h, 24 h, 48 h and 72 h).The mRNA and protein levels of FoxM1 were detected by real-time PCR and Western blot.FoxM1 siRNA was transfected into K562 cells with 0.015μmol/L HHT after 6 h.After 72 h incubation, the cell proliferation was detected by cell counting and soft agar assay, and the proportion of apoptotic K562 cells was determined by flow cytometry.The expression of c-Myc and Sp1 were detected by real-time PCR and Western blot.RESULTS:FoxM1 expression was reduced time-dependently and dose-dependently, suggesting that HHT mediated the downregulation of FoxM1 in K562 cells.In K562 cells, treatment with FoxM1 siRNA and HHT inhibited the cell proliferation and promoted the apoptosis significantly.Therefore, inhibition of FoxM1 sensitized leukemia K562 cells to HHT.The expression of c-Myc and Sp1 was positively regulated by FoxM1. CONCLUSION:HHT inhibits Forkhead box protein M1 expression in K562 cells.Inhibition of FoxM1 sensitizes K562 cells to HHT.