Linked Life Data

15203383

Source:http://linkedlifedata.com/resource/pubmed/id/15203383

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2004-6-18
pubmed:abstractText
Vitamin E derivative, RRR-alpha-tocopheryl succinate (vitamin E succinate, VES), is a potent pro-apoptotic agent, inducing apoptosis by restoring both transforming growth factor-beta (TGF-beta) and Fas (CD95) apoptotic signaling pathways that contribute to the activation of c-Jun N-terminal kinase (JNK)-mediated apoptosis. Objectives of these studies were to characterize signaling events involved in the pro-apoptotic actions of a naturally occurring form of vitamin E, delta-tocotrienol, and a novel vitamin E analog, alpha-tocopherol ether acetic acid analog [alpha-TEA; 2,5,7,8-tetramethyl-2R-(4R,8R,12-trimethyltridecyl)chroman-6-yloxyacetic acid]. Like VES, alpha-TEA and delta-tocotrienol induced estrogen-nonresponsive MDA-MB-435 and estrogen-responsive MCF-7 human breast cancer cells to undergo high levels of apoptosis in a concentration- and time-dependent fashion. Like VES, the two compounds induced either no or lower levels of apoptosis in normal human mammary epithelial cells and immortalized but nontumorigenic human MCF-10A cells. The pro-apoptotic mechanisms triggered by the structurally distinct alpha-TEA and delta-tocotrienol were identical to those previously reported for VES, that is, alpha-TEA- and delta-tocotrienol-induced apoptosis involved up-regulation of TGF-beta receptor II expression and TGF-beta-, Fas- and JNK-signaling pathways. These data provide a better understanding of the anticancer actions of a dietary form of vitamin E (delta-tocotrienol) and a novel nonhydrolyzable vitamin E analog (alpha-TEA).
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0163-5581
pubmed:author
pubmed:copyrightInfo
Copyright 2004 Lawrence Erlbaum Associates, Inc.
pubmed:issnType
Print
pubmed:volume
48
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
95-105
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:15203383-Anticarcinogenic Agents, pubmed-meshheading:15203383-Antigens, CD95, pubmed-meshheading:15203383-Apoptosis, pubmed-meshheading:15203383-Blotting, Western, pubmed-meshheading:15203383-Breast Neoplasms, pubmed-meshheading:15203383-Cell Division, pubmed-meshheading:15203383-Cell Line, Tumor, pubmed-meshheading:15203383-Cell Survival, pubmed-meshheading:15203383-Dose-Response Relationship, Drug, pubmed-meshheading:15203383-Drug Screening Assays, Antitumor, pubmed-meshheading:15203383-Female, pubmed-meshheading:15203383-Gene Expression Regulation, Neoplastic, pubmed-meshheading:15203383-Humans, pubmed-meshheading:15203383-Receptors, Transforming Growth Factor beta, pubmed-meshheading:15203383-Signal Transduction, pubmed-meshheading:15203383-Tocopherols, pubmed-meshheading:15203383-Vitamin E
pubmed:year
2004
pubmed:articleTitle
Pro-apoptotic mechanisms of action of a novel vitamin E analog (alpha-TEA) and a naturally occurring form of vitamin E (delta-tocotrienol) in MDA-MB-435 human breast cancer cells.
pubmed:affiliation
Division of Nutrition/A2703, University of Texas at Austin, 78712, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.