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In the present study, in order to investigate the anticancer effects ofO-desmethylangolensin (O-DMA) on human hepatocellular carcinoma Hep3B cells, wefirst examined the antiproliferative effect of O-DMA. When Hep3B cells were treatedwith O-DMA at various concentrations (5-200 µM) for 24, 48 or 72 h, cell proliferationdecreased significantly in a dose- and time-dependent manner. Moreover, O-DMAexposure at the IC50 concentration for 72 h arrested cells at the G2/M phase,which was accompanied by a reduction in CDK1, and an increase in cyclin A and B.Under the same conditions, O-DMA significantly increased the number of sub-G1phase cells. Additionally, an Annexin V assay revealed that exposure to O-DMAaffected the rate of cell apoptosis. O-DMA caused the downregulation of Bcl-2and upregulation of Bax, which led to cytochrome c release from the mitochondriaand activation of caspase-3. Taken together, these data suggest that O-DMA exhibitsanticancer activity by arresting the cell cycle at G2/M phase and causing mitochondrial-dependentapoptosis in Hep3B cells.

international journal of molecular medicine

Anticancer effects of O-desmethylangolensin are mediated through cell cycle arrest at the G2/M phase and mitochondrial-dependent apoptosis in Hep3B human hepatocellular carcinoma cells