Apoptosis of HL-60 human leukemia cells induced by Asiatic acid through modulation of B-cell lymphoma 2 family proteins and the mitogen-activated protein kinase signaling pathway

• DOI: 10.3892/mmr.2015.3534
• Publication Date: 2015-03-24T08:45:53Z
• Authors: QIULING WU; TINGTING LV; YAN CHEN; LU WEN; JUNLI ZHANG; XUDONG JIANG; FANG LIU
• Keywords: Propidium iodide; Survivin

The toxicities of conventional chemotherapeutic agents to normal cells restrict their dosage and clinical efficacy in acute leukemia; therefore, it is important develop novel chemotherapeutics, including natural products, which selectively target cancer‑specific pathways. present study aimed explore the effect chemopreventive agent asiatic acid (AA) on proliferation apoptotic rate leukemia cell line HL‑60 investigated mechanisms underlying its anti‑tumor activity. AA was evaluated using MTT assay. Annexin V‑fluorescein isothiocyanate/propidium iodide double staining followed by flow cytometric analysis as well Hoechst 33258 were used analyze cells. Furthermore, changes survivin, B‑cell lymphoma 2 (Bcl‑2), myeloid 1 (Mcl‑1), extracellular signal‑regulated kinase (ERK), c‑Jun N‑terminal (JNK) p38 expressions detected western blot analysis. blocked growth a dose‑ time‑dependent manner. IC50‑value 46.67±5.08 µmol/l for 24 h. induced apoptosis dose‑dependent manner, inhibited presence Z‑DEVD‑FMK, specific inhibitor caspase. anti‑apoptotic proteins Bcl‑2, Mcl‑1 survivin downregulated Concurrently, ERK phosphorylation while JNK not affected. In conclusion, indicated that pathways, modulation Bcl‑2 family key regulators response AA.