Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2002-3-6
pubmed:abstractText
Elucidation of the mechanisms underlying potential anticancer drugs continues and unraveling these mechanisms would not only provide a conceptual framework for drug design but also promote use of natural products for chemotherapy. To further evaluate the efficacy of the anticancer activity of 1'-acetoxychavicol acetate (ACA), this study investigates the underlying mechanisms by which ACA induces death of Ehrlich ascites tumor cells. ACA treatment induced loss of cell viability, and Western blotting analysis revealed that the compound stimulated tyrosine phosphorylation of several proteins with 27 and 70 kDa proteins being regulated in both dose- and time-dependent manner prior to loss of viability. Protein tyrosine kinase inhibitor herbimycin A moderately protected cells from ACA-induced toxicity. In addition, cellular glutathione and protein sulfydryl groups were also significantly reduced both dose- and time-dependently during evidence of cell death. Replenishing thiol levels by antioxidant, N-acetylcysteine (NAC), an excellent supplier of glutathione and precursor of glutathione, substantially recovered the viability loss, but the recovery being time-dependent, as late addition of NAC (at least 30 min after ACA addition to cultures) was, however, ineffective. Addition of NAC to ACA treated cultures also abolished tyrosine phosphorylation of the 27 kDa protein. These results, at least partly, identify cellular sulfhydryl groups and protein tyrosine phosphorylation as targets of ACA cytotoxicity in tumor cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/1'-acetoxychavicol acetate, http://linkedlifedata.com/resource/pubmed/chemical/Anticarcinogenic Agents, http://linkedlifedata.com/resource/pubmed/chemical/Benzoquinones, http://linkedlifedata.com/resource/pubmed/chemical/Benzyl Alcohols, http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors, http://linkedlifedata.com/resource/pubmed/chemical/Glutathione, http://linkedlifedata.com/resource/pubmed/chemical/Lactams, Macrocyclic, http://linkedlifedata.com/resource/pubmed/chemical/Quinones, http://linkedlifedata.com/resource/pubmed/chemical/Sulfhydryl Compounds, http://linkedlifedata.com/resource/pubmed/chemical/Terpenes, http://linkedlifedata.com/resource/pubmed/chemical/Tyrosine, http://linkedlifedata.com/resource/pubmed/chemical/herbimycin
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0009-2797
pubmed:author
pubmed:issnType
Print
pubmed:day
20
pubmed:volume
139
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
215-30
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:11823008-Animals, pubmed-meshheading:11823008-Anticarcinogenic Agents, pubmed-meshheading:11823008-Benzoquinones, pubmed-meshheading:11823008-Benzyl Alcohols, pubmed-meshheading:11823008-Blotting, Western, pubmed-meshheading:11823008-Carcinoma, Ehrlich Tumor, pubmed-meshheading:11823008-Cell Survival, pubmed-meshheading:11823008-Dose-Response Relationship, Drug, pubmed-meshheading:11823008-Drug Interactions, pubmed-meshheading:11823008-Enzyme Inhibitors, pubmed-meshheading:11823008-Glutathione, pubmed-meshheading:11823008-Lactams, Macrocyclic, pubmed-meshheading:11823008-Oxidation-Reduction, pubmed-meshheading:11823008-Phosphorylation, pubmed-meshheading:11823008-Quinones, pubmed-meshheading:11823008-Sulfhydryl Compounds, pubmed-meshheading:11823008-Terpenes, pubmed-meshheading:11823008-Time Factors, pubmed-meshheading:11823008-Tumor Cells, Cultured, pubmed-meshheading:11823008-Tyrosine
pubmed:year
2002
pubmed:articleTitle
Involvement of protein tyrosine phosphorylation and reduction of cellular sulfhydryl groups in cell death induced by 1' -acetoxychavicol acetate in Ehrlich ascites tumor cells.
pubmed:affiliation
Department of Food and Human Health Sciences, Graduate School of Human Life Science, Osaka City University, 3-3-138 Sugimoto, Sumiyoshi-ku, Osaka 558-8585, Japan.
pubmed:publicationType
Journal Article