Linked Life Data

17970076

Source:http://linkedlifedata.com/resource/pubmed/id/17970076

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5A
pubmed:dateCreated
2007-10-31
pubmed:abstractText
Apoptosis is a physiological mechanism for eliminating malignant cells, including cancer cells, without eliciting damage to normal cells or surrounding tissues. Here, we report that rhein (4,5-dihydroxyanthraquinone-2-carboxylic acid), a major constituent in the rhizome of rhubarb, induced apoptosis of human nasopharyngeal carcinoma (NPC) cells. Rhein induced apoptosis in NPC cells as demonstrated by increased nuclear condensation and DNA fragmentation. Moreover, for the first time in NPC cells it was demonstrated that the pathway involved in rhein-induced apoptosis is caspase-dependent, presumably through the endoplasmic reticulum (ER) stress pathway, as shown by an increase in the levels of glucose-regulated protein 78 (GRP 78), PKR-like ER kinase (PERK), activating transcription factor 6 (A TF6) and CCAA TIenhancer-binding protein homologous protein (CHOP) as well as the activation of caspase-3, -8, -9 and -12. This increased susceptibility to ER stress-induced apoptosis may be due to an increased accumulation of reactive oxygen species (ROS). Rapid accumulation of calcium (Ca2+) and a decrease in the mitochondrial membrane potential (MMP) were also observed. Cytochrome c and apoptosis-inducing factor (AIF) were released upon treatment with rhein. Taken together, these results suggest that ER stress and Ca2+-dependent mitochondrial death pathway may be involved in rhein-induced apoptosis in NPC cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0250-7005
pubmed:author
pubmed:issnType
Print
pubmed:volume
27
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3313-22
pubmed:meshHeading
pubmed:articleTitle
Rhein induces apoptosis through induction of endoplasmic reticulum stress and Ca2+-dependent mitochondrial death pathway in human nasopharyngeal carcinoma cells.
pubmed:affiliation
School of Medical Laboratory Science and Biotechnology, China Medical University, Taichung, Taiwan, ROC.
pubmed:publicationType
Journal Article