rdf:type |
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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.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-10398166,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/20620960-9079683
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pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Jun
|
pubmed:issn |
1097-4164
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pubmed:author |
|
pubmed:copyrightInfo |
Copyright (c) 2010 Elsevier Inc. All rights reserved.
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pubmed:issnType |
Electronic
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pubmed:day |
25
|
pubmed:volume |
38
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
908-15
|
pubmed:dateRevised |
2011-8-1
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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.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
|