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  4. Allicin induces p53-mediated autophagy in Hep G2 human liver cancer cells
 
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Allicin induces p53-mediated autophagy in Hep G2 human liver cancer cells

Journal
Journal of Agricultural and Food Chemistry
Journal Volume
60
Journal Issue
34
Pages
8363-8371
Date Issued
2012
Author(s)
Chu Y.-L.
Ho C.-T.
Chung J.-G.
Rajasekaran R.
Sheen L.-Y.  
DOI
10.1021/jf301298y
URI
https://scholars.lib.ntu.edu.tw/handle/123456789/413557
URL
https://www.scopus.com/inward/record.uri?eid=2-s2.0-84865650394&doi=10.1021%2fjf301298y&partnerID=40&md5=d4025e7d680b1d6ba1d92f89c6360741
Abstract
Garlic has been used throughout history for both culinary and medicinal purpose. Allicin is a major component of crushed garlic. Although it is sensitive to heat and light and easily metabolized into various compounds such as diallyl disulfide, diallyl trisulfide, and diallyl sulfide, allicin is still a major bioactive compound of crushed garlic. The mortality of hepatocellular carcinoma is quite high and ranks among the top 10 cancer-related deaths in Taiwan. Although numerous studies have shown the cancer-preventive properties of garlic and its components, there is no study on the effect of allicin on the growth of human liver cancer cells. In this study, we focused on allicin-induced autophagic cell death in human liver cancer Hep G2 cells. Our results indicated that allicin induced p53-mediated autophagy and inhibited the viability of human hepatocellular carcinoma cell lines. Using Western blotting, we observed that allicin decreased the level of cytoplasmic p53, the PI3K/mTOR signaling pathway, and the level of Bcl-2 and increased the expression of AMPK/TSC2 and Beclin-1 signaling pathways in Hep G2 cells. In addition, the colocalization of LC3-II with MitoTracker-Red (labeling mitochondria), resulting in allicin-induced degradation of mitochondria, could be observed by confocal laser microscopy. In conclusion, allicin of garlic shows great potential as a novel chemopreventive agent for the prevention of liver cancer. ? 2012 American Chemical Society.
Subjects
allicin
autophagy
Hep G2 cells
LC3-II
p53
SDGs

[SDGs]SDG3

Other Subjects
allicin; Autophagic cells; Autophagy; Bioactive compounds; Chemopreventive agents; Colocalization; Confocal laser microscopy; Diallyl disulfide; Diallyl sulfide; Diallyl trisulfides; Hepatocellular carcinoma; Hepatocellular carcinoma cell; Human liver; Human liver cancer cells; LC3-II; Liver cancers; p53; Signaling pathways; Western blotting; Cell culture; Cell death; Degradation; Pigments; Sulfur compounds; Diseases; allicin; antineoplastic agent; apoptosis regulatory protein; BECN1 protein, human; MAP1LC3A protein, human; membrane protein; microtubule associated protein; MTOR protein, human; sulfinic acid derivative; target of rapamycin kinase; tuberin; tumor suppressor protein; apoptosis; article; autophagy; cell survival; drug effect; HepG2 cell line; high performance liquid chromatography; human; metabolism; methodology; mitochondrial membrane potential; phagosome; physiology; signal transduction; synthesis; tandem mass spectrometry; tumor suppressor gene; Anticarcinogenic Agents; Apoptosis; Apoptosis Regulatory Proteins; Autophagy; Cell Survival; Chromatography, High Pressure Liquid; Genes, p53; Hep G2 Cells; Humans; Membrane Potential, Mitochondrial; Membrane Proteins; Microtubule-Associated Proteins; Phagosomes; Signal Transduction; Sulfinic Acids; Tandem Mass Spectrometry; TOR Serine-Threonine Kinases; Tumor Suppressor Proteins; Allium sativum
Type
journal article

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