[Effect of arsenic trioxide on differentiation induction of chronic myeloid leukemia k562 cells and its potential mechanism].

OBJECTIVE

This study was to explore the effect of arsenic trioxide (ATO; As(2)O(3)) on differentiation of chronic myeloid leukemia K562 cells and its potential mechanism.

METHODS

ATO with different concentration (0.1, 0.5, 1.0, 2.0, 5.0 µmol/L) were used to treat K562 cells, and MTT assay was used to detect the growth level of K562 cells; Benzidine staining was applied to measure the change of hemoglobin content; flow cytometry (FCM) was conducted to detect the expression of CD41 and GPA on K562 cells; RT-PCR and Western blot were used to measure the mRNA expression of BTG1 and TAL1 and the protein expression of BTG1 and TAL1, respectively.

RESULTS

ATO significantly inhibited the growth of K562 with dose- and time- dependent manners by benzidine staining, the positive rate of K562 cells induced by ATO reached to 17.63% ± 1.18%, which was significantly higher than that of control (2.87% ± 0.63%) (P < 0.01), and GPA, as the specific marker of erythroid cell differentiation, achieved 68.46% ± 3.67%, while it in control was 3.39% ± 0.84% (P < 0.01), besides, the CD41 expression of megakaryocyte increased but not so obvious as GPA. Meanwhile, the differentiation-related transcriptional factors TAL1 and BTG1 mRNA and the corresponding proteins were expressed more highly.

CONCLUSION

ATO can induce the differentiation of K562 cells into erythroid cells and megakaryocyte, which is associated with up-regulation of the related transcription factors TAL1 and BTG1.