Linked Life Data

21206973

Source:http://linkedlifedata.com/resource/pubmed/id/21206973

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2011-2-3
pubmed:abstractText
It is well known that the response of cancer cells to chemotherapeutic drugs involves the activation of apoptotic pathways. Benzyl isothiocyanate (BITC) is an important compound found in plant food and has been shown to have anti-cancer effects on human cancer cells, but its effect on prostate cancer cells in vitro remains unknown. The aim of the present study was to investigate the effects of BITC on DU 145 human prostate cancer cells in order to clarify whether a time/concentration range for optimal BITC-induced apoptosis exists and to find the associated signaling pathway. Cell morphological changes, percentage of cell viability, DNA damage and apoptosis in DU 145 cells were examined by phase-contrast microscopy, flow cytometric assay, 4',6-diamidine-20-phenylindole dihydrochloride staining, comet assay and Western blotting analysis. The results indicate that BITC induces cell morphological changes, decreases the percentage of viable cells (induction of cell cytotoxicity), and induces DNA damage and apoptosis in DU 145 cells in a time- and dose-dependent manner. Flow cytometric assays indicated that BITC promoted reactive oxygen species and Ca2+ productions and decreased the levels of mitochondrial membrane potential (?Ym), while the pre-treatment with N-acetylcysteine caused an increase in the percentage of viable cells. BITC also promoted caspase-3, -8 and -9 activities. Furthermore, when cells were pre-treated with the caspase-3 inhibitor and then treated with BITC, this led to an increase in the percentage of viable cells. Confocal laser microscopy examination indicated that BITC promoted the expression of AIF and Endo G, which were released from the mitochondria in DU 145 cells. In conclusion, BITC induces apoptosis in DU 145 cells through the release of AIF and Endo G from the mitochondria and also promotes caspase-3 activation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1791-2423
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
38
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
787-96
pubmed:meshHeading
pubmed-meshheading:21206973-Acetylcysteine, pubmed-meshheading:21206973-Adenocarcinoma, pubmed-meshheading:21206973-Antineoplastic Agents, pubmed-meshheading:21206973-Apoptosis, pubmed-meshheading:21206973-Apoptosis Inducing Factor, pubmed-meshheading:21206973-Caspases, pubmed-meshheading:21206973-Cell Line, Tumor, pubmed-meshheading:21206973-Dose-Response Relationship, Drug, pubmed-meshheading:21206973-Drug Evaluation, Preclinical, pubmed-meshheading:21206973-Endodeoxyribonucleases, pubmed-meshheading:21206973-Gene Expression Regulation, Neoplastic, pubmed-meshheading:21206973-Humans, pubmed-meshheading:21206973-Isothiocyanates, pubmed-meshheading:21206973-Male, pubmed-meshheading:21206973-Membrane Potential, Mitochondrial, pubmed-meshheading:21206973-Mitochondria, pubmed-meshheading:21206973-Models, Biological, pubmed-meshheading:21206973-Prostatic Neoplasms, pubmed-meshheading:21206973-Signal Transduction
pubmed:year
2011
pubmed:articleTitle
The roles of AIF and Endo G in the apoptotic effects of benzyl isothiocyanate on DU 145 human prostate cancer cells via the mitochondrial signaling pathway.
pubmed:affiliation
Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung 404, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't