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Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi ; 28(11): 1129-32, 2012 Nov.
Artigo em Chinês | MEDLINE | ID: mdl-23127398

RESUMO

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.


Assuntos
Antineoplásicos/farmacologia , PTEN Fosfo-Hidrolase/fisiologia , Piperazinas/farmacologia , Inibidores de Proteínas Quinases/farmacologia , Proteínas Tirosina Quinases/antagonistas & inibidores , Pirimidinas/farmacologia , Transdução de Sinais/efeitos dos fármacos , Benzamidas , Proteína-Tirosina Quinases de Adesão Focal/análise , Proteína-Tirosina Quinases de Adesão Focal/genética , Proteínas de Fusão bcr-abl/genética , Humanos , Mesilato de Imatinib , Células K562 , Invasividade Neoplásica , PTEN Fosfo-Hidrolase/análise , PTEN Fosfo-Hidrolase/genética , RNA Mensageiro/análise
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