A potential chemotherapeutic drug to treat hepatocellular carcinoma
A number of dietary compounds possess anti-cancer properties. These dietary compounds may modify the activity of specific targets that control cell proliferation and apoptosis. Galangin could inhibit the methoxyresorufin O-demethylase activity of CYP1A2, CYP1A1 and P-form phenolsulfotransferase. Galangin induced apoptosis in several cancer cell lines and arrested the cell cycle, modulated the expression of cycline/cdk, and decreased Bcl-2. It was suggested that galangin may be a potential anti-tumor agent. However, the mechanism by which galangin exerts its anti-tumor activity is unknown.
A research article to be published on July 21, 2010 in the World Journal of Gastroenterology addresses this question. This is the first study to report that galangin mediates apoptosis through a mitochondrial pathway.
Their data demonstrated that (1) galangin induces HCC cell apoptosis by triggering Bax translocation to the mitochondria; (2) galangin-treated HCC cells causes the release of AIF and cytochrome c into the cytosol from the mitochondria; and (3) overexpression of BclDŽ attenuated galangin-induced HepG2 cells apoptosis, while down-regulated Bcl-2 expression enhanced galangin to induce cell apoptosis.
Understanding the mechanism by which galangin induces apoptosis may lead to its use as an anti-cancer treatment of HCC. This study may represent a future potential chemotherapeutic drug in the treatment of HCC with galangin.
Source: http://www.sciencedaily.com/releases/2010/07/1007300910ǭ.htm