title: [Up-regulation of NKG2D ligand ULBP2 by matrine in K562 cells and the underlying molecular mechanisms].
abstract: OBJECTIVE
  To probe matrine acting on natural killer cell (NK) activating receptor NKG2D ligands expression in CML cell line K562 and its underlying molecular mechanism.
  
  
  METHODS
  The expression of NKG2D ligands (major histocompatibility complex class I chain-related molecule A or B (MICA/B), UL16-binding proteins (ULBP) 1, 2, and 3 on K562 cells were analyzed before and after treated with matrine by FCM. The cytotoxic sensitivity of K562 to NK cell was detected by FCM after CFSE staining at different effect-to-target (E/T) cell ratios. The expression of signal transduction and transcriptional activator 3 (STAT3) protein as well as phosphorylated STAT3 (p-STAT3) were detected by western blot.
  
  
  RESULTS
  After treatment with matrine, ULBP1 and ULBP2 expression, especially ULBP2 on K562 cells significantly increased, with mean fluorescence intensity (MFI) increasing to 615 and 1614 by 220 and 615 in the untreated cells, respectively. There was no significant change for MICA or ULBP3 expression. Matrine enhanced the susceptibility of K562 cells to NK-mediated cell lysis. At the ratio of E/T with 5:1, the proportion of the killed K562 cells increased to 32.8%, 38.1% and 40.5%, respectively (after 0.2, 0.5 and 0.8 mg/ml matrine treatment) by 29.2% in the untreated cells. The phosphorylated STAT3 protein, but not STAT3 protein, was significantly inhibited by matrine treatment in K562 cells.
  
  
  CONCLUSIONS
  Matrine induced the expression of NKG2D ligands in K562cells and enhanced the cytotoxicity of NK cells against K562, which was closely related to the inhibition of STAT3 activity in K562 cell.
authors.affiliation: Department of Hematology, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
authors.forename: Lingdi
authors.initials: L
authors.lastname: Ma
authors.affiliation: Department of Hematology, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
authors.forename: Zhichao
authors.initials: Z
authors.lastname: Zhu
authors.affiliation: Department of Hematology, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
authors.forename: Xuzhang
authors.initials: X
authors.lastname: Lu
authors.affiliation: Department of Hematology, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
authors.forename: Lijia
authors.initials: L
authors.lastname: Jiang
authors.affiliation: Department of Hematology, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
authors.forename: Min
authors.initials: M
authors.lastname: Zhou
authors.affiliation: Department of Hematology, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
authors.forename: Sixuan
authors.initials: S
authors.lastname: Qian
authors.affiliation: Department of Hematology, the First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
authors.forename: Jianyong
authors.initials: J
authors.lastname: Li
mesh_terms: D000470:Alkaloids / Q000494:pharmacology; D058851:GPI-Linked Proteins / Q000276:immunology; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins / Q000276:immunology*; D020014:K562 Cells; D011807:Quinolizines / Q000494:pharmacology; D015398:Signal Transduction; D015854:Up-Regulation / Q000187:drug effects; D000093842:Matrines
chemical_list: D000470:Alkaloids; D058851:GPI-Linked Proteins; D036341:Intercellular Signaling Peptides and Proteins; D011807:Quinolizines; C423230:ULBP2 protein, human; D000093842:Matrines