A research article to be published on June 21, 2009 in the World Journal of Gastroenterology addresses this question. The research team led by Professor Yan Li from Shengjing Hospital of China Medical University studied the growth inhibitory effects of Alisol B acetat and determined its mechanism of antitumor activity in human gastric cancer cell line SGC7901.
Professor Li and his colleagues found that Alisol B acetat could inhibit the proliferation of SGC7901 cell in a time and dose dependent manner. Among the various phases of cell cycle, the percentage of cells in S phase was significantly decreased, while the percentage of cells in G1 phase was increased. Flow cytometry assay also showed Alisol B acetate had positive effect on apoptosis. Typical apoptotic morphology such as condensation and fragmentation of nuclei and formation of apoptotic bodies could be observed through electron microscope and phase-contrast microscope. Further investigating the molecular mechanism behind Alisol B acetat -induced apoptosis, cells treated with Alisol B acetat underwent a rapid loss of mitochondrial transmembrane potential, activition of caspase-3, -9, upregulation of Apaf-1 and Bax, and inhibition of the PI3K/Akt in a time-dependent manner.
The researches domenstrated for the first time that Alisol B acetate induced human gastric cancer apoptosis through regulation of mitochondrial and PI3K/AKT signaling pathways Their research results indicate that Alisol B acetate might be used to treat gastric cancer , one of the most common cancers worldwide. By knowing the mechanism of action of Alisol B acetate, it may provide a new therapeutic option, as a potential anticancer agent, in the treatment of gastric cancer.
More information: Xu YH, Zhao LJ, Li Y. Alisol B acetate induces apoptosis of SGC7901 cells via mitochondrial and phosphatidylinositol 3-kinases/Akt signaling pathways. World J Gastroenterol 2009; 15(23): 2870-2877. www.wjgnet.com/1007-9327/15/2870.asp
Source: World Journal of Gastroenterology (news : web)