title: [Effect of tyrosine kinase inhibitor imatinib mesylate   on K562 cell invasion by PTEN pathway].
abstract: OBJECTIVE
  To investigate the effect of tyrosine kinase inhibitor imatinib mesylate on the PTEN signaling pathway and the cell invasion in K562 cells.
  
  
  METHODS
  K562 cells were treated with different concentrations of imatinib mesylate. After different time periods,  the mRNA levels of BCR/ABL,  PTEN and FAK were detected by real-time fluorescent quantitative PCR (FQ-PCR) to analyze their relationships. The protein level of FAK was detected by immunocytochemistry. The cell invasive ability was examined by Transwell (Boyden chamber)  assay.
  
  
  RESULTS
  In the initial 36 h,  the expression level of PTEN mRNA was up-regulated and the FAK mRNA was down-regulated with the reduction of BCR/ABL fusion gene expression and the cell invasive ability of K562 cells was inhibited by 2 μg/mL imatinib mesylate. 48 h later,  the PTEN mRNA expression level decreased and the FAK mRNA expression level was elevated with the restore of BCR/ABL fusion gene. BCR/ABL mRNA level presented a positive correlation with PTEN mRNA expression level,  and a negative correlation with FAK mRNA.
  
  
  CONCLUSIONS
  Tyrosine kinase inhibitor imatinib mesylate can regulate PTEN/FAK pathway and inhibit the leukemia K562 cell invasive ability via restraining BCR/ABL fusion gene.
authors.affiliation: Department of Hematology, Baoding First Hospital, Baoding, China.
authors.forename: Zhi-yong
authors.initials: ZY
authors.lastname: Cheng
authors.forename: Wen-tong
authors.initials: WT
authors.lastname: Liang
authors.forename: Xiao-yan
authors.initials: XY
authors.lastname: Yan
authors.forename: Jian-she
authors.initials: JS
authors.lastname: Wan
authors.forename: Yong-sheng
authors.initials: YS
authors.lastname: Bian
authors.forename: Ping
authors.initials: P
authors.lastname: Bai
authors.forename: Li-qing
authors.initials: LQ
authors.lastname: Liang
authors.forename: Jun-qing
authors.initials: JQ
authors.lastname: Jie
authors.forename: Ai-ming
authors.initials: AM
authors.lastname: Li
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology*; D001549:Benzamides; D051416:Focal Adhesion Protein-Tyrosine Kinases / Q000032:analysis / Q000235:genetics; D016044:Fusion Proteins, bcr-abl / Q000235:genetics; D006801:Humans; D000068877:Imatinib Mesylate; D020014:K562 Cells; D009361:Neoplasm Invasiveness; D051059:PTEN Phosphohydrolase / Q000032:analysis / Q000235:genetics / Q000502:physiology*; D010879:Piperazines / Q000494:pharmacology*; D047428:Protein Kinase Inhibitors / Q000494:pharmacology*; D011505:Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors*; D011743:Pyrimidines / Q000494:pharmacology*; D012333:RNA, Messenger / Q000032:analysis; D015398:Signal Transduction / Q000187:drug effects*
chemical_list: D000970:Antineoplastic Agents; D001549:Benzamides; D010879:Piperazines; D047428:Protein Kinase Inhibitors; D011743:Pyrimidines; D012333:RNA, Messenger; D000068877:Imatinib Mesylate; D011505:Protein-Tyrosine Kinases; D051416:Focal Adhesion Protein-Tyrosine Kinases; D016044:Fusion Proteins, bcr-abl; D051059:PTEN Phosphohydrolase; C494929:PTEN protein, human