title: [Gene Expression Profile of Apoptosis in Leukemia Cells Induced by Hsp90 Selective inhibitor 17-AAG].
abstract: OBJECTIVE
  To investigate the apoptotic effects of Hsp90 selective inhibitor 17-AAG on human leukemia HL-60 and NB4 cells and analyse its possible mechanism.
  
  
  METHODS
  CCK-8 assay was used to quantify the growth inhibition of cells after exposure to 17-AAG for 24 hours. Flow cytometrve with annexin V/propidium iodide staining was used to detect apoptosis of leukemia cells. Then Western blot was used to detect the activation of apoptosis related protein caspase-3 and PARP level. Gene expression profile of NB4 cells treated with 17-AAG was analyzed with real-time PCR arrays.
  
  
  RESULTS
  The inhibition of leukemia cell proliferation displayed a dose-dependent manner. Annexin V assay, cell cycle analysis and activation of PARP demonstrate that 17-AAG induced apoptosis leukemia cells. Real-time PCR array analysis showed that expression of 56 genes significantly up-regulated and expression of 23 genes were significantly down-regulated after 17-AAG treatment.
  
  
  CONCLUSIONS
  The 17-AAG can inhibit the proliferation and induce the apoptosis of leukemia cells. After leukemia cells are treated with 17-AAG, the significant changes of apoptosis-related genes occured, and the cell apoptosis occurs via activating apoptosis related signaling pathway.
authors.affiliation: Department of Children Hospital, Affiliated Hospital of Sozhou University, Sochou 215006, Jiangsu Province, China.
authors.forename: Na-Na
authors.initials: NN
authors.lastname: Wang
authors.affiliation: Department of Children Hospital, Affiliated Hospital of Sozhou University, Sochou 215006, Jiangsu Province, China.
authors.forename: Zhi-Heng
authors.initials: ZH
authors.lastname: Li
authors.affiliation: Department of Children Hospital, Affiliated Hospital of Sozhou University, Sochou 215006, Jiangsu Province, China.
authors.forename: Yan-Fang
authors.initials: YF
authors.lastname: Tao
authors.affiliation: Department of Children Hospital, Affiliated Hospital of Sozhou University, Sochou 215006, Jiangsu Province, China.
authors.forename: Li-Xiao
authors.initials: LX
authors.lastname: Xu
authors.affiliation: Department of Children Hospital, Affiliated Hospital of Sozhou University, Sochou 215006, Jiangsu Province, China.
authors.forename: Jian
authors.initials: J
authors.lastname: Pan
authors.affiliation: Department of Children Hospital, Affiliated Hospital of Sozhou University, Sochou 215006, Jiangsu Province, China. E-mail: hsy139@126.com.
authors.forename: Shao-Yan
authors.initials: SY
authors.lastname: Hu
mesh_terms: D017209:Apoptosis; D016227:Benzoquinones / Q000494:pharmacology*; D053148:Caspase 3 / Q000378:metabolism; D002453:Cell Cycle; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D015536:Down-Regulation; D018922:HL-60 Cells; D018841:HSP90 Heat-Shock Proteins / Q000037:antagonists & inhibitors*; D006801:Humans; D047029:Lactams, Macrocyclic / Q000494:pharmacology*; D007938:Leukemia / Q000378:metabolism*; D011065:Poly(ADP-ribose) Polymerases / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction; D015398:Signal Transduction; D059467:Transcriptome
chemical_list: D016227:Benzoquinones; D018841:HSP90 Heat-Shock Proteins; D047029:Lactams, Macrocyclic; C112765:tanespimycin; D011065:Poly(ADP-ribose) Polymerases; C505407:CASP3 protein, human; D053148:Caspase 3