期刊
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
卷 31, 期 3, 页码 726-730出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/ijmm.2013.1230
关键词
apoptosis; cell cycle arrest; daidzein; Hep3B cells; O-desmethylangolensin
资金
- Basic Research Program through the National Research Foundation of Korea (NRF)
- Ministry of Education, Science and Technology [2012-0006811, 2012-041653]
In the present study, in order to investigate the anticancer effects of O-desmethylangolensin (O-DMA) on human hepatocellular carcinoma Hep3B cells, we first examined the antiproliferative effect of O-DMA. When Hep3B cells were treated with O-DMA at various concentrations (5-200 mu M) for 24, 48 or 72 h, cell proliferation decreased significantly in a dose- and time-dependent manner. Moreover, O-DMA exposure 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-G1 phase cells. Additionally, an Annexin V assay revealed that exposure to O-DMA affected the rate of cell apoptosis. O-DMA caused the downregulation of Bcl-2 and upregulation of Bax, which led to cytochrome c release from the mitochondria and activation of caspase-3. Taken together, these data suggest that O-DMA exhibits anticancer activity by arresting the cell cycle at G2/M phase and causing mitochondrial-dependent apoptosis in Hep3B cells.
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