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|標題:||The anti-metastatic efficacy of beta-ionone and the possible mechanisms of action in human hepatocarcinoma SK-Hep-1 cells||作者:||Huang, C.S.
|關鍵字:||beta-Ionone;Metastasis;Nm23-H1;Focal adhesion kinase;Rho GTPase;focal adhesion kinase;hepatocellular-carcinoma cells;cancer-cells;signal-transduction;rho-gtpases;in-vitro;metastasis;migration;invasion;suppressor||Project:||British Journal of Nutrition||期刊/報告no：:||British Journal of Nutrition, Volume 107, Issue 5, Page(s) 631-638.||摘要:||
beta-Ionone (BI), a precursor for carotenoids, is widely distributed in fruit and vegetables. Recent in vitro studies have demonstrated the potential anti-metastatic effects of BI, but the mechanisms underlying such actions are not clear. Because liver cancer is the most endemic cancer in Taiwan and in a large region of the world, we hereby investigate the anti-metastatic effects of BI and its mechanisms of actions in a highly metastatic human hepatocarcinoma SK-Hep-1 cells. We show that incubation of cells with BI (1-50 mu M) for 24 and 48 h significantly inhibited cell invasion, migration and adhesion. Mechanistically, incubation of cells with BI (1-50 mu M) for 24 h resulted in the following: (1) significant inhibition of matrix metalloproteinase (MMP)-2, MMP-9 and urokinase-type plasminogen activator activities, (2) up-regulation of protein expression of the tissue inhibitor of matrix metalloproteinase (TIMP)-1, TIMP-2 and plasminogen activator inhibitor-1, (3) down-regulation of the expression of migration-related proteins, including focal adhesion kinase (FAK), phosphorylated form of FAK, Rho, Rac1 and Cdc42 and (4) up-regulation of the expression of nm23-H1 protein (P<0.05). Overall, the results show that BI effectively inhibits the metastasis of SK-Hep-1 cells, and this effect involves the regulation of gene expression and signal pathways related to invasion and migration.
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