ABSTRACT
OBJECTIVE: To explore the effect and molecular mechanism of Piceatannol on malignant biological characteristics of acute myeloid leukemia (AML) cells. METHODS: HL60, U937, HL60/ADR and U937/ADR cells were treated with different concentrations of Piceatannol. CCK-8 assay was used to detect cell proliferation. Cell apoptosis was detected by flow cytometry with Annexin V/PI double staining. The protein expressions of apoptosis, autophagy and related signaling pathways were detected by Western blot. Real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression changes of drug resistance genes in drug-resistant AML cell lines. RESULTS: The activity of HL60 and U937 cells could be inhibited by Piceatannol and induced apoptosis. When Piceatannol interfered with AML cells for 24 h, the ratio of autophagy marker LC3-II/LC3-I increased with the increase of concentration (r=0.672ï¼ r=0.549). When Piceatannol interfered with AML cells for 48 h, the expression of Bcl-2 protein was down-regulated and caspase-3 was hydrolyzed and activated. At the same time, the activation level of Akt/NF-κB signaling pathway was inhibited to induce programmed death of AML cells. Piceatannol can also down-regulate the expression of MRP1 and gradually weaken the chemotherapy resistance of AML drug-resistant cell lines, but it has a weak effect on the expression of BCRP and almost no effect on MDR1. CONCLUSION: Piceatannol can inhibit the proliferation of AML cells and induce programmed death, which may be related to the inhibition of Akt/NF-κB signaling pathway, the hydrolysis of caspase-3 and the down-regulation of Bcl-2 protein expression, and the suppression of the expression of some drug resistance genes.
