Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2011-5-9
pubmed:abstractText
MicroRNAs are widely dysregulated in various cancers and integrated into tumorigenic programs as either oncogenes or tumor suppressor genes. Here, we show that miR-26b, which is down-regulated in human breast cancer specimens and cell lines, impairs viability and triggers apoptosis of human breast cancer MCF7 cells. SLC7A11 is identified as a direct target of miR-26b and its expression is remarkably increased in both breast cancer cell lines and clinical samples. Furthermore, SLC7A11 silence mimics miR-26b-aroused viability impairment and apoptosis in MCF7 cells. Our studies reveal a protective role of miR-26b in the molecular etiology of human breast cancer by promoting apoptosis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1873-3468
pubmed:author
pubmed:copyrightInfo
Copyright © 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
pubmed:issnType
Electronic
pubmed:day
6
pubmed:volume
585
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1363-7
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
MicroRNA-26b is underexpressed in human breast cancer and induces cell apoptosis by targeting SLC7A11.
pubmed:affiliation
Institute of Health Sciences, Shanghai Jiao Tong University School of Medicine (SJTU-SM), Chinese Academy of Sciences (CAS), Shanghai, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't