C‑Myc inhibitor 10058‑F4 increases the efficacy of dexamethasone on acute lymphoblastic leukaemia cells.

The long‑term survival rate in paediatric acute lymphoblastic leukaemia (ALL) exceeds 80%; however, the outcome of adult ALL remains to be poor. Glucocorticoids (GCs) are the preferred drugs in the traditional treatment of ALL patients. In the anti‑leukaemia molecular mechanisms of GCs, c‑Myc inhibition serves a critical role. In the present study, a c‑Myc inhibitor that increased the sensitivity to GCs in NALM6 cells of the B‑cell‑ALL cell line and CEM cells of the T‑cell‑ALL cell line was investigated. The data demonstrated that 10058‑F4, a c‑Myc inhibitor, increased the growth inhibition, G0/G1 phase arrest and apoptosis of the NALM6 and CEM cells as induced by dexamethasone (DXM), a type of GC. Additionally, 10058‑F4 reinforced the decreased expressions of c‑Myc, cyclin‑dependent kinase (CDK)‑4 and CDK6 in the NALM6 and CEM cells treated with DXM. These findings indicated that DXM in combination with the c‑Myc inhibitor 10058‑F4 may be a novel, potent therapeutic strategy for the treatment of ALL.