Source:http://linkedlifedata.com/resource/pubmed/id/21550168
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2011-5-31
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pubmed:abstractText |
MicroRNA (miR)-143 and -145 were down-regulated in human bladder cancer T24 cells. The enforced expression of miR-143 induced growth-suppression in T24 cells through down-regulation of ERK5 and Akt expression at translational level, and chemically-modified synthetic miR-143 (miR-143/BP) exhibited a greater growth inhibitory effect than wild-type miR-143. In addition, the synthetic miR-143/BP induced apoptotic cell death in some of the transfected cells. Furthermore, co-treatment with the synthetic miR-143/BP and cisplatin showed the additive growth-suppressing effect on T24 cells. These findings suggest that the chemically-modified synthetic miR-143 functions as a tumor suppressor in T24 cells by targeting ERK5 and/or Akt.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1872-7980
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pubmed:author | |
pubmed:copyrightInfo |
Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.
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pubmed:issnType |
Electronic
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pubmed:day |
28
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pubmed:volume |
307
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
211-20
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pubmed:meshHeading |
pubmed-meshheading:21550168-Base Sequence,
pubmed-meshheading:21550168-Blotting, Western,
pubmed-meshheading:21550168-Cell Line, Tumor,
pubmed-meshheading:21550168-DNA Primers,
pubmed-meshheading:21550168-Humans,
pubmed-meshheading:21550168-MicroRNAs,
pubmed-meshheading:21550168-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:21550168-Urinary Bladder Neoplasms
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pubmed:year |
2011
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pubmed:articleTitle |
MicroRNA-143 functions as a tumor suppressor in human bladder cancer T24 cells.
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pubmed:affiliation |
The United Graduate School of Veterinary Sciences, Gifu University, Yanagido, Gifu, Japan. o5104401@edu.gifu-u.ac.jp
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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