The pterocarpanquinone LQB‑118 compound induces apoptosis of cytarabine‑resistant acute myeloid leukemia cells

Acute myeloid leukemia (AML) is a complex hematological disorder characterized by blockage of differentiation and high proliferation rates progenitors. Anthracycline cytarabine‑based therapy has remained the standard treatment for AML over last four decades. Although this strategy increased survival rates, patients often develop resistance to these drugs. Despite efforts understand mechanisms underlying cytarabine resistance, there have been few advances in field. The present study developed an in vitro cell line model resistant (HL‑60R), identified chromosomal aberrations karyotype evaluation potential molecular chemoresistance. Cytarabine decreased viability, as determined MTT assay, induced death cycle arrest parental HL‑60 line, revealed Annexin V/propidium iodide (PI) staining PI DNA incorporation, respectively, whereas no change was observed HL‑60R line. In addition, exhibited higher tumorigenic capacity vivo compared with Notably, reduction tumor volume detected mice treated inoculated cells. western blotting that protein expression levels Bcl‑2, X‑linked inhibitor apoptosis (XIAP) c‑Myc were upregulated cells those cells, along predominant nuclear localization p50 p65 subunits NF‑κB Furthermore, antitumor effect LQB‑118 pterocarpanquinone investigated; compound apoptosis, viability decrease XIAP cytarabine‑resistant Taken together, data indicated acquired multifactorial process, involving aberrations, differential signaling pathways. could be alternative therapeutic approach treat