title: Allicin induces p53-mediated autophagy in Hep G2 human liver cancer cells.
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.
authors.affiliation: Institute of Food Science and Technology, National Taiwan University , Taipei, Taiwan, Republic of China.
authors.forename: Yung-Lin
authors.initials: YL
authors.lastname: Chu
authors.forename: Chi-Tang
authors.initials: CT
authors.lastname: Ho
authors.forename: Jing-Gung
authors.initials: JG
authors.lastname: Chung
authors.forename: Raghu
authors.initials: R
authors.lastname: Rajasekaran
authors.forename: Lee-Yan
authors.initials: LY
authors.lastname: Sheen
mesh_terms: D016588:Anticarcinogenic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism; D001343:Autophagy / Q000187:drug effects*; D000071186:Beclin-1; D002470:Cell Survival / Q000187:drug effects; D002851:Chromatography, High Pressure Liquid / Q000379:methods; D004220:Disulfides; D016158:Genes, p53 / Q000502:physiology*; D056945:Hep G2 Cells / Q000187:drug effects; D006801:Humans; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008565:Membrane Proteins / Q000378:metabolism; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D010588:Phagosomes / Q000187:drug effects; D015398:Signal Transduction / Q000187:drug effects; D013441:Sulfinic Acids / Q000138:chemical synthesis / Q000494:pharmacology*; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism; D053719:Tandem Mass Spectrometry; D000077005:Tuberous Sclerosis Complex 2 Protein; D025521:Tumor Suppressor Proteins / Q000378:metabolism
chemical_list: D016588:Anticarcinogenic Agents; D051017:Apoptosis Regulatory Proteins; C491997:BECN1 protein, human; D000071186:Beclin-1; D004220:Disulfides; C477012:MAP1LC3A protein, human; D008565:Membrane Proteins; D008869:Microtubule-Associated Proteins; D013441:Sulfinic Acids; C000624653:TSC2 protein, human; D000077005:Tuberous Sclerosis Complex 2 Protein; D025521:Tumor Suppressor Proteins; C006452:allicin; C546842:MTOR protein, human; D058570:TOR Serine-Threonine Kinases