July 30, 2010 Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide, particularly in China. However, HCC remains one of the more difficult cancers to treat. It is important to screen for new anti-cancer drugs.
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 Bcl-2 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.
Other social bookmarking and sharing tools:
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
- Zhang HT, Luo H, Wu J, Lan LB, Fan DH, Zhu KD, Chen XY, Wen M, Liu HM. Galangin induces apoptosis of hepatocellular carcinoma cells via the mitochondrial pathway. World Journal of Gastroenterology, 2010; 16 (27): 3377 DOI: 10.3748/wjg.v16.i27.3377
Note: If no author is given, the source is cited instead.