Abstract:
:Casticin, a polymethoxyflavone, has been reported to exert anticancer activities. The objectives of this study were to examine the molecular mechanisms by which casticin induces the growth inhibition and cell cycle arrest in human hepatocellular carcinoma (HCC) cells. The HCC cell lines Hep G2 and PLC/PRF/5 were cultured in vitro. The growth inhibitory effects of casticin were evaluated using clonogenic assays. The distribution of phases in the cell cycle was analyzed using flow cytometry (FCM) analysis with propidium iodide (PI) staining. Multiple molecular techniques, such as western blotting and gene transfection, were used to explore the molecular mechanisms of action. Our data demonstrated that casticin significantly inhibited cell viability and colony formation in HCC cells. Furthermore, it induced cell cycle arrest in the G2/M phase. Casticin inhibited phosphorylation of the FOXO3a protein and decreased the expression of FoxM1 and its downstream genes, such as cyclin-dependent kinase (CDK1), cdc25B and cyclin B and increased the expression of p27KIP1. Silencing of FOXO3a expression by small interfering RNA (siRNA) transfection clearly attenuated the inhibitory effects of casticin on FOXM1 expression and cell growth. Our findings provided clear evidence that casticin induces growth suppression and cell cycle arrest through inhibition of FOXO3a phosphorylation causing inactivation of FOXM1 in HCC cells.
journal_name
Oncol Repjournal_title
Oncology reportsauthors
He L,Yang X,Cao X,Liu F,Quan M,Cao Jdoi
10.3892/or.2012.2076subject
Has Abstractpub_date
2013-01-01 00:00:00pages
103-8issue
1eissn
1021-335Xissn
1791-2431journal_volume
29pub_type
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