title: Allicin inhibits cell growth and induces apoptosis in U87MG human glioblastoma             cells through an ERK-dependent pathway.
abstract: Allicin, the main flavor compound in garlic, has anti-carcinogenic activities             in a range of cancer cells, however, the underlying molecular mechanisms are not             completely understood. This study examined the effect of allicin on the cell viability             of U87MG human glioma cells along with its molecular mechanisms of induction of             cell death. Apoptosis was determined by TUNEL and Hoechst 33258 staining as well             as by western blot analysis. Allicin inhibited the cell viability of U87MG human             glioma cells in a dose- and time-dependent manner. Allicin-induced inhibition             of cell viability was due to apoptosis of cells. The mechanisms of apoptosis were             found to involve the mitochondrial pathway of Bcl-2/Bax, the MAPK/ERK signaling             pathway and antioxidant enzyme systems. These results suggest that allicin can             serve as a novel chemotherapeutic candidate for the treatment of glioblastoma             multiforme.
authors.affiliation: Department of Neurosurgery, Pusan National University Hospital,                     Pusan National University School of Medicine, Busan 602-739, Republic                     of Korea.
authors.forename: Jae Hun
authors.initials: JH
authors.lastname: Cha
authors.forename: Yoon Ji
authors.initials: YJ
authors.lastname: Choi
authors.forename: Seung Heon
authors.initials: SH
authors.lastname: Cha
authors.forename: Chang Hwa
authors.initials: CH
authors.lastname: Choi
authors.forename: Won Ho
authors.initials: WH
authors.lastname: Cho
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology; D000970:Antineoplastic Agents / Q000494:pharmacology*; D000975:Antioxidants / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects*; D002070:Butadienes / Q000494:pharmacology; D020169:Caspases / Q000378:metabolism; D002374:Catalase / Q000494:pharmacology; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects*; D048430:Cell Shape / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D004220:Disulfides; D048049:Extracellular Signal-Regulated MAP Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D005909:Glioblastoma; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D020935:MAP Kinase Signaling System / Q000187:drug effects; D009570:Nitriles / Q000494:pharmacology; D010766:Phosphorylation; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D011725:Pyridines / Q000494:pharmacology; D013441:Sulfinic Acids / Q000494:pharmacology*; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D000970:Antineoplastic Agents; D000975:Antioxidants; C494826:BAX protein, human; D002070:Butadienes; D004220:Disulfides; D007093:Imidazoles; D009570:Nitriles; D019253:Proto-Oncogene Proteins c-bcl-2; D011725:Pyridines; D013441:Sulfinic Acids; C113580:U 0126; D051028:bcl-2-Associated X Protein; C006452:allicin; D002374:Catalase; D048049:Extracellular Signal-Regulated MAP Kinases; D020169:Caspases; C093642:SB 203580; D000111:Acetylcysteine