FoxM1 promotes development of AML by regulating Bcl-2 expression
10.3969/j.issn.1000-4718.2016.08.007
- VernacularTitle:FoxM1靶向调控 bcl－2促进急性髓系白血病发生
- Author:
Jin CHEN
;
Xiaoming WANG
;
Minran ZHOU
;
Ting SUN
;
Zhongmin CHEN
;
Chunyan CHEN
- Publication Type:Journal Article
- Keywords:
Acute myeloid leukemia;
Forkhead box M1;
Bcl-2
- From:
Chinese Journal of Pathophysiology
2016;32(8):1383-1388
- CountryChina
- Language:Chinese
-
Abstract:
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 .
