Abstract

Objective To investigate the effects of 5-aminimidazole-4-formamide nucleotide(AICAR), a monophosphate kinase(AMPK)agonist, on proliferation, differentiation and apoptosis of chronic myeloid leukemia K562 cell line. Methods CCK-8 assay was used to detect K562 cell proliferation; Wright-Giemsa staining and light microscopy were used to observe of K562 cell morphology; flow cytometry was used to detect K562 cell surface differentiation antigens CD7, CD11b, CD34, HLA-DR; FITC Annexin-V/PI double staining was used to detect early apoptosis of K562 cell; and immunocytochemistry was used to detect the expression of wild-type P53 protein. Results AICAR inhibited the proliferation of K562 cells at different concentrations(1.0~2.0 mmol/L)and different time(24-72 h), and the inhibition dependented on time and dose.AICAR can promote the expression of wild-type p53 protein.There was no significant difference in the expression of CD7, CD11b, CD34 and HLA-DR surface antigen between K562 cells treated with 2.0 mmol/LAICAR and control group(P>0.05). Conclusion AICAR inhibited the proliferation of K562 cells with time-and dose-dependent .The mechanism may be related to the up-regulation of wild-type P53 protein expression. Key words: 5- amino imidazole- 4 formamide nucleotide; K562 cell; Apoptosis

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