|Title:||Allicin induces anti-human liver cancer cells through the p53 gene modulating apoptosis and autophagy||Authors:||Chu Y.-L.
|Keywords:||Allicin;apoptosis;autophagy;p53;reactive oxygen species||Issue Date:||2013||Journal Volume:||61||Journal Issue:||41||Start page/Pages:||9839-9848||Source:||Journal of Agricultural and Food Chemistry||Abstract:||
Hepatocellular carcinoma (HCC) is the most prevalent type of liver cancer globally and ranks first among the cancer-related mortalities in Taiwan. This study aims to understand the modes of cell death mechanism induced by allicin, a major phytochemical of crushed garlic, in human hepatoma cells. Our earlier study indicated that allicin induced autophagic cell death in human HCC Hep G2 (p53wild type) cells, whereas in the present study, allicin induced apoptotic cell death through caspase-dependent and caspase-independent pathways by reactive oxygen species (ROS) overproduction in human HCC Hep 3B (p53 mutation) cells. To gain insight into the cell death mechanism in p53 knocked down Hep G2, we silenced the p53 gene using siRNA-mediated silencing. Allicin treatment induced apoptotic cell death in p53 knocked down Hep G2 cells similar to that of Hep 3B cells. These results suggest that allicin induced cell death in human hepatoma cells through either autophagy or apoptosis and might be a potential novel complementary gene therapeutic agent for the treatment of apoptosis-resistant cancer cells. ? 2013 American Chemical Society.
|Appears in Collections:||食品科技研究所|
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