[Effect of tyrosine kinase inhibitor imatinib mesylate on K562 cell invasion by PTEN pathway]

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2012 Nov;28(11):1129-32.
[Article in Chinese]

Abstract

Aim: 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.

Conclusion: Tyrosine kinase inhibitor imatinib mesylate can regulate PTEN/FAK pathway and inhibit the leukemia K562 cell invasive ability via restraining BCR/ABL fusion gene.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Benzamides
  • Focal Adhesion Protein-Tyrosine Kinases / analysis
  • Focal Adhesion Protein-Tyrosine Kinases / genetics
  • Fusion Proteins, bcr-abl / genetics
  • Humans
  • Imatinib Mesylate
  • K562 Cells
  • Neoplasm Invasiveness
  • PTEN Phosphohydrolase / analysis
  • PTEN Phosphohydrolase / genetics
  • PTEN Phosphohydrolase / physiology*
  • Piperazines / pharmacology*
  • Protein Kinase Inhibitors / pharmacology*
  • Protein-Tyrosine Kinases / antagonists & inhibitors*
  • Pyrimidines / pharmacology*
  • RNA, Messenger / analysis
  • Signal Transduction / drug effects*

Substances

  • Antineoplastic Agents
  • Benzamides
  • Piperazines
  • Protein Kinase Inhibitors
  • Pyrimidines
  • RNA, Messenger
  • Imatinib Mesylate
  • Protein-Tyrosine Kinases
  • Focal Adhesion Protein-Tyrosine Kinases
  • Fusion Proteins, bcr-abl
  • PTEN Phosphohydrolase
  • PTEN protein, human