RESUMO
<p><b>OBJECTIVE</b>To explore the possible mechanism underlaying interference of epihopin on the proliferation of AML KG-1a cells by inhibiting the Wnt/β-catenin signaling pathway, so as to prvide the experimental basis for development of drug to treat the AML.</p><p><b>METHODS</b>A total of 50 c57BL/6 mice were randomy divided into 5 group:blank control, model control, high, medium and low dose of epihopin. Except the blank control group, the KG-1a cells were injected in abdominal cavity of 4 groups for the establishment of model. The mice in high, middle and low dose groups were injected intramuscularly with 80, 40 and 20 mg/kg of epihopin respectively, while the mice in blank control and model control group were injected intramuscularly with saline. The Western blot was used to detect the expression of S phase kinase-related protein 2(SKP-2), β-catenin, E-cadherin and poly-(ADP ribose) polymerase (PARP); the spectrophotometry was used to detect the activity of caspase 3 and procaspase-3, the flow cytometry was used to detect the cell cycle distribution and the apoptotic rate of KG-1a cells treated with epihopin.</p><p><b>RESULTS</b>The epihopin could enhance the activity of caspase 3, decrease the level of procaspase 3; also could up-regulate the expression of E-acadherin and down-regulate the expression of SKP-2 and β-catenin; and could increase the expression of PARP in dose-dependent manner. After KG-1a cels were treated with epihopin, the apoptosis rate of cells significantly increased, the KG-1a cells were arrested in G/G phase, therefore the growth of KG-1a cells was significantly inhibited.</p><p><b>CONCLUSION</b>The epihopin can dose-dependently split PARP to induce the apoptosis of KG-1a cells, its mechanism may relate with inhibition of Wnt/β-catenin signaling pathway and its down-stream-related gene expression.</p>