@article{kwak_parthenolide_2014,
	title = {Parthenolide induces apoptosis by activating the mitochondrial and death receptor pathways and inhibits {FAK}-mediated cell invasion},
	volume = {385},
	issn = {1573-4919},
	doi = {10.1007/s11010-013-1822-4},
	abstract = {The natural product parthenolide induces apoptosis in cancer cells. However, the mechanism of apoptosis in ovarian cancer cells exposed to parthenolide is not clear. In addition, it is unclear whether parthenolide-induced apoptosis is mediated by the formation of reactive oxygen species and the depletion of GSH contents, and the effect of parthenolide on the invasion and migration of human epithelial ovarian cancer cells has not been studied. Therefore, we investigated the effects of parthenolide exposure on apoptosis, cell adhesion, and migration using the human epithelial ovarian carcinoma cell lines OVCAR-3 and SK-OV-3. The results suggest that parthenolide may induce apoptotic cell death in ovarian carcinoma cell lines by activating the mitochondrial pathway and the caspase-8- and Bid-dependent pathways. The apoptotic effect of parthenolide appears to be mediated by the formation of reactive oxygen species and the depletion of GSH. Parthenolide inhibited fetal bovine serum-induced cell adhesion and migration of OVCAR-3 cells, possibly through the suppression the focal adhesion kinase-dependent activation of cytoskeletal-associated components. Therefore, parthenolide might be beneficial in the treatment of epithelial ovarian adenocarcinoma and combination therapy.},
	number = {1-2},
	journal = {Molecular and cellular biochemistry},
	author = {Kwak, Sang Won and Park, Eon Sub and Lee, Chung Soo},
	month = jan,
	year = {2014},
	pmid = {24065392},
	keywords = {Apoptosis, Apoptosis Regulatory Proteins, Caspases, Cell Adhesion, Cell Line, Tumor, Cell Movement, Cell Survival, DNA Damage, Enzyme Activation, Focal Adhesion Protein-Tyrosine Kinases, Glutathione, Humans, Membrane Potential, Mitochondrial, Mitochondria, Neoplasm Invasiveness, Oxidants, Reactive Oxygen Species, Receptors, Death Domain, Sesquiterpenes, Signal Transduction},
	pages = {133--144}
}

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However, the mechanism of apoptosis in ovarian cancer cells exposed to parthenolide is not clear. In addition, it is unclear whether parthenolide-induced apoptosis is mediated by the formation of reactive oxygen species and the depletion of GSH contents, and the effect of parthenolide on the invasion and migration of human epithelial ovarian cancer cells has not been studied. Therefore, we investigated the effects of parthenolide exposure on apoptosis, cell adhesion, and migration using the human epithelial ovarian carcinoma cell lines OVCAR-3 and SK-OV-3. The results suggest that parthenolide may induce apoptotic cell death in ovarian carcinoma cell lines by activating the mitochondrial pathway and the caspase-8- and Bid-dependent pathways. The apoptotic effect of parthenolide appears to be mediated by the formation of reactive oxygen species and the depletion of GSH. Parthenolide inhibited fetal bovine serum-induced cell adhesion and migration of OVCAR-3 cells, possibly through the suppression the focal adhesion kinase-dependent activation of cytoskeletal-associated components. Therefore, parthenolide might be beneficial in the treatment of epithelial ovarian adenocarcinoma and combination therapy.","number":"1-2","journal":"Molecular and cellular biochemistry","author":[{"propositions":[],"lastnames":["Kwak"],"firstnames":["Sang","Won"],"suffixes":[]},{"propositions":[],"lastnames":["Park"],"firstnames":["Eon","Sub"],"suffixes":[]},{"propositions":[],"lastnames":["Lee"],"firstnames":["Chung","Soo"],"suffixes":[]}],"month":"January","year":"2014","pmid":"24065392","keywords":"Apoptosis, Apoptosis Regulatory Proteins, Caspases, Cell Adhesion, Cell Line, Tumor, Cell Movement, Cell Survival, DNA Damage, Enzyme Activation, Focal Adhesion Protein-Tyrosine Kinases, Glutathione, Humans, Membrane Potential, Mitochondrial, Mitochondria, Neoplasm Invasiveness, Oxidants, Reactive Oxygen Species, Receptors, Death Domain, Sesquiterpenes, Signal Transduction","pages":"133--144","bibtex":"@article{kwak_parthenolide_2014,\n\ttitle = {Parthenolide induces apoptosis by activating the mitochondrial and death receptor pathways and inhibits {FAK}-mediated cell invasion},\n\tvolume = {385},\n\tissn = {1573-4919},\n\tdoi = {10.1007/s11010-013-1822-4},\n\tabstract = {The natural product parthenolide induces apoptosis in cancer cells. However, the mechanism of apoptosis in ovarian cancer cells exposed to parthenolide is not clear. In addition, it is unclear whether parthenolide-induced apoptosis is mediated by the formation of reactive oxygen species and the depletion of GSH contents, and the effect of parthenolide on the invasion and migration of human epithelial ovarian cancer cells has not been studied. Therefore, we investigated the effects of parthenolide exposure on apoptosis, cell adhesion, and migration using the human epithelial ovarian carcinoma cell lines OVCAR-3 and SK-OV-3. The results suggest that parthenolide may induce apoptotic cell death in ovarian carcinoma cell lines by activating the mitochondrial pathway and the caspase-8- and Bid-dependent pathways. The apoptotic effect of parthenolide appears to be mediated by the formation of reactive oxygen species and the depletion of GSH. 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