title: Induction of apoptosis and inhibition of invasion in choriocarcinoma JEG-3 cells by α-calendic acid and β-calendic acid.
abstract: Alfa-calendic acid and β-calendic acid, geometric and positional isomers of linolenic acid were previously shown to possess potent anticancer properties. In this study, we found that α-calendic acid and β-calendic acid could induce apoptosis and suppress invasion of human choriocarcinoma JEG-3 cells in vitro. Treatment with α-calendic acid and β-calendic acid significantly increased oxidative stress in human choriocarcinoma JEG-3 cells detected by the level of reactive oxygen species (ROS), lipid peroxidation production malondialdehyde (MDA), glutathione (GSH) and the effects of antioxidants NAC and α-tocopherol. Furthermore, oxidative stress activated the phosphorylation of p38MAPK. SB203580, a selective p38MAPK inhibitor, blocked the apoptosis induced by α-calendic acid and β-calendic acid by upregulating Bcl-2/Bax ratio and inhibition of the activation of Caspase-3 and Caspase-9. SB20350 also partially abrogated the cell invasion effects of α-calendic acid and β-calendic acid. These results suggested that α-calendic acid and β-calendic acid induced apoptosis and inhibited invasion in JEG-3 cells by activation of oxidative stress pathways and subsequent activation of P38MAPK.
authors.affiliation: Liaoning Key Laboratory of Food Biological Technology, School of Food Science and Technology, Dalian Polytechnic University, No. 1 Qinggongyuan, Gan District, Dalian 116034, China.
authors.forename: Qian
authors.initials: Q
authors.lastname: Li
authors.forename: Han
authors.initials: H
authors.lastname: Wang
authors.forename: Shuhong
authors.initials: S
authors.lastname: Ye
authors.forename: Shan
authors.initials: S
authors.lastname: Xiao
authors.forename: Yuping
authors.initials: Y
authors.lastname: Xie
authors.forename: Xiao
authors.initials: X
authors.lastname: Liu
authors.forename: Jihui
authors.initials: J
authors.lastname: Wang
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology; D000972:Antineoplastic Agents, Phytogenic / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D020169:Caspases / Q000235:genetics / Q000378:metabolism; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000187:drug effects; D005231:Fatty Acids, Unsaturated / Q000494:pharmacology*; D005260:Female; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects*; D005978:Glutathione / Q000378:metabolism; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D015227:Lipid Peroxidation / Q000187:drug effects; D008315:Malondialdehyde / Q000378:metabolism; D018384:Oxidative Stress; D011725:Pyridines / Q000494:pharmacology; D017382:Reactive Oxygen Species / Q000819:agonists* / Q000378:metabolism; D015398:Signal Transduction; D013237:Stereoisomerism; D024502:alpha-Tocopherol / Q000494:pharmacology; D050998:bcl-2 Homologous Antagonist-Killer Protein / Q000235:genetics / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000235:genetics / Q000378:metabolism; D048051:p38 Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism
chemical_list: D000972:Antineoplastic Agents, Phytogenic; C494826:BAX protein, human; D005231:Fatty Acids, Unsaturated; D007093:Imidazoles; D011725:Pyridines; D017382:Reactive Oxygen Species; D050998:bcl-2 Homologous Antagonist-Killer Protein; D051028:bcl-2-Associated X Protein; D008315:Malondialdehyde; C428441:calendic acid; D048051:p38 Mitogen-Activated Protein Kinases; D020169:Caspases; D005978:Glutathione; D024502:alpha-Tocopherol; C093642:SB 203580; D000111:Acetylcysteine
keywords: Apoptosis; Conjugated linolenic acid (CLN); Invasion