title: STAT3 signaling pathway is involved in decitabine induced biological phenotype regulation of acute myeloid leukemia cells.
abstract: OBJECTIVE
  This study aimed to investigate the role of signal transduction and transcriptional activator STAT3 and relevant signaling pathway in the DAC regulated biological phenotype of AML cells.
  
  
  METHODS
  The effect of DAC at different concentrations on the proliferation of HL-60 cells was determined. After DAC treatment for 48 h, the killing capability of NK cells against HL-60 cells and the protein expressions of STAT3, JAK1, JAK2, SOCS-1 and SOCS-3 were evaluated.
  
  
  RESULTS
  DAC markedly inhibited the proliferation of HL-60 cells. After the treatment of 48 hr with 0.2, 0.5 and 1.0 mol/L DAC, the HL-60 viability was reduced by 25±13%, 39±8% and 50±7% (P<0.01), respectively, and the early apoptosis rate was increased to 24.77±7.5%, 27.1±4.48% and 30.53±3.93%, respectively (control: 3.11±0.12%, P<0.01). DAC up-regulated the expression of MICA/B, ULBP-1 and ULBP-3 in HL-60 cells, and increased the killing activity of NK cells to HL-60 cells. DAC significantly induced the apoptosis of HL-60 cells and up-regulated the expression of NKG2D ligands in a dose dependent manner. Western blot assay showed the protein expression of STAT3, JAK, JAK2, phosphorylated STAT3, phosphorylated JAK1 and phosphorylated JAK2 decreased, while that of SOCS-1 and SOCS-3 increased in HL-60 cells after DAC treatment.
  
  
  CONCLUSIONS
  In HL-60 cells, DAC can markedly inhibit their proliferation and up-regulate the expression of NKG2D ligands, and DAC also increase the cytotoxicity of NK cells to HL-60 cells, which may be related to the STAT3 related signaling pathway.
authors.affiliation: Laboratory Center, Changzhou No. 2 People's Hospital, Affiliated Hospital of Nanjing Medical University No. 29 Xinglong Lane, Changzhou 213000, China.
authors.forename: Zhichao
authors.initials: Z
authors.lastname: Zhu
authors.affiliation: Department of Hematology, Changzhou No. 2 People's Hospital, Affiliated Hospital of Nanjing Medical University No. 188 Gehu Middle Road, Changzhou 213000, China.
authors.forename: Xuzhang
authors.initials: X
authors.lastname: Lu
authors.affiliation: Laboratory Center, Changzhou No. 2 People's Hospital, Affiliated Hospital of Nanjing Medical University No. 29 Xinglong Lane, Changzhou 213000, China.
authors.forename: Lijia
authors.initials: L
authors.lastname: Jiang
authors.affiliation: Laboratory Center, Changzhou No. 2 People's Hospital, Affiliated Hospital of Nanjing Medical University No. 29 Xinglong Lane, Changzhou 213000, China.
authors.forename: Xiao
authors.initials: X
authors.lastname: Sun
authors.affiliation: Laboratory Center, Changzhou No. 2 People's Hospital, Affiliated Hospital of Nanjing Medical University No. 29 Xinglong Lane, Changzhou 213000, China.
authors.forename: Haijun
authors.initials: H
authors.lastname: Zhou
authors.affiliation: Department of Hematology, Changzhou No. 2 People's Hospital, Affiliated Hospital of Nanjing Medical University No. 188 Gehu Middle Road, Changzhou 213000, China.
authors.forename: Zhuxia
authors.initials: Z
authors.lastname: Jia
authors.affiliation: Department of Hematology, Changzhou No. 2 People's Hospital, Affiliated Hospital of Nanjing Medical University No. 188 Gehu Middle Road, Changzhou 213000, China.
authors.forename: Xiuwen
authors.initials: X
authors.lastname: Zhang
authors.affiliation: Department of Laboratory Medicine, Huizhou No. 3 People's Hospital, Affiliated Hospital of Guangzhou Medical University No. 1 Xuebei Street, Qiaodong Road, Huizhou 615000, China.
authors.forename: Lingdi
authors.initials: L
authors.lastname: Ma
keywords: Decitabine; NKG2D ligand; SOCSs; STAT3; acute myeloid leukemia; natural killer cells