Study on the sensitivity of STAT3 gene expression in the treatment of imatinib to chronic myeloid leukemia / 安徽医科大学学报

ABSTRACT

Objective To observe the expression of signal transducer and activator of transcription (STAT3) in chronic myeloid leukemia cells K562 and analyze the influence of these changes to the cell proliferation,differentiation and drug resistance.Methods We constructed recombinant eukaryotic expression vector siRNA-STAT3,and transfected them into K562 cells with the help of lipofactamine 3000.Then stable monoclonal cells would be screened by puromycin and validated by Western blot.Inhibition rate of the cell growth to imatinib(IM) was determined by MTT method.Meanwhile,the related protein of BCR/ABL fusion protein was detected.Results Compared with the control group,low expression of STAT3 in the K562 cell group using IM treatment had a high inhibition rate,under different concentrations,the inhibition rate was statistically significant(P ＜ 0.05).While in the high expression of STAT3 cells,at the same concentration gradient under the action of IM,and the differences between groups were also statistically significant(P ＜ 0.05).However,there was no statistically significant difference of the inhibition rate in the two control groups.We also detected the similar expression levels of the related protein of BCR/ABL fusion protein,P53,HAUSP and PTEN.Conclusion Low expression of the STAT3 protein enhances the sensitivity of K562 cells to IM,which may result in a further reduction in the subsequent resistance of the K562 cells to IM treatment by inhibiting the STAT3 protein.