Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2010-7-12
pubmed:abstractText
Tumor progression shares many characteristics with the process of epithelial-to-mesenchymal transition (EMT). Cells that have undergone an EMT are known to have an increased resistance to apoptosis. CD95/Fas is an apoptosis-inducing receptor expressed on many tissues and tumor cells. During tumor progression CD95 is frequently downregulated, and tumor cells lose apoptosis sensitivity. miR-200 microRNAs repress both the EMT-inducing ZEB1 and ZEB2 transcription factors. We now demonstrate that miR-200c sensitizes cells to apoptosis mediated by CD95. We have identified the apoptosis inhibitor FAP-1 as a target for miR-200c. FAP-1 was demonstrated to be responsible for the reduced sensitivity to CD95-mediated apoptosis in cells with inhibited miR-200. The identification of FAP-1 as an miR-200c target provides a molecular mechanism to explain both the downregulation of CD95 expression and the reduction in sensitivity of cells to CD95-mediated apoptosis that is observed in the context of reduced miR-200 expression during tumor progression.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-10398166, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-10537175, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-10647931, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-10918185, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-11106428, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-11172597, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-11274632, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-11290551, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-11598958, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-11683408, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-12655293, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-12724420, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-14504390, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-15907590, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-16187021, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-16306044, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-16498403, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-16888780, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-17482535, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-17585049, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-17804704, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-17982484, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-18160445, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-18376396, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-18381893, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-18836476, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-19167326, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-19221491, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-7536343, http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-9079683
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1097-4164
pubmed:author
pubmed:copyrightInfo
Copyright (c) 2010 Elsevier Inc. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
25
pubmed:volume
38
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
908-15
pubmed:dateRevised
2011-8-1
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
miR-200c regulates induction of apoptosis through CD95 by targeting FAP-1.
pubmed:affiliation
The Ben May Department for Cancer Research, The University of Chicago, Chicago, IL 60637, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural