Acute lymphoblastic leukemia (ALL) is the most common malignant disorder in children and intensive combination therapy has markedly improved patient prognosis. However, efficacy of the treatment still fails in 10-15% of patients. Glucocorticoids (GCs) such as prednisone and dexamethasone (DEX) are essential drugs used for ALL chemotherapy, and the response to GC treatment is a strong independent factor of ALL prognosis. In the present study, we examined the mechanism of GC resistance of B-cell precursor ALL (BCP-ALL). As determined by RT-qPCR and western blot analyses, GC treatment upregulated glucocorticoid receptor (GR) protein and Bcl-2-interacting mediator of cell death (BCL2L11, BIM) protein expression, resulting in apoptosis of a GC-sensitive BCP-ALL cell line, but not of a GC-resistant BCP-ALL cell line as shown by flow cytometry. GR was downregulated in a DEX-resistant BCP-ALL cell line which was induced by treatment of cells with increasing concentrations of DEX. Importantly, expression levels of miR-142-3p and miR-17∼92 cluster were upregulated in the BCP-ALL cell line with acquired DEX resistance as examined by RT-qPCR. Our results suggest that interference of miR-142-3p and miR-17∼92 may overcome the resistance of BCP-ALL to GCs.
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