Linked Life Data

20543867

Source:http://linkedlifedata.com/resource/pubmed/id/20543867

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
31
pubmed:dateCreated
2010-8-5
pubmed:abstractText
Epithelial to mesenchymal transition (EMT) is a key step toward metastasis. MCF7 breast cancer cells conditionally expressing the EMT master regulator SNAI1 were used to identify early expressed microRNAs (miRNAs) and their targets that may contribute to the EMT process. Potential targets of miRNAs were identified by matching lists of in silico predicted targets and of inversely expressed mRNAs. MiRNAs were ranked based on the number of predicted hits, highlighting miR-661, a miRNA with so far no reported role in EMT. MiR-661 was found required for efficient invasion of breast cancer cells by destabilizing two of its predicted mRNA targets, the cell-cell adhesion protein Nectin-1 and the lipid transferase StarD10, resulting, in turn, in the downregulation of epithelial markers. Reexpression of Nectin-1 or StarD10 lacking the 3'-untranslated region counteracted SNAI1-induced invasion. Importantly, analysis of public transcriptomic data from a cohort of 295 well-characterized breast tumor specimen revealed that expression of StarD10 is highly associated with markers of luminal subtypes whereas its loss negatively correlated with the EMT-related, basal-like subtype. Collectively, our non-a priori approach revealed a nonpredicted link between SNAI1-triggered EMT and the down-regulation of Nectin-1 and StarD10 through the up-regulation of miR-661, which may contribute to the invasion of breast cancer cells and poor disease outcome.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1476-5594
pubmed:author
pubmed:issnType
Electronic
pubmed:day
5
pubmed:volume
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4436-48
pubmed:meshHeading
pubmed-meshheading:20543867-Breast Neoplasms, pubmed-meshheading:20543867-Cell Adhesion Molecules, pubmed-meshheading:20543867-Cell Dedifferentiation, pubmed-meshheading:20543867-Epithelial Cells, pubmed-meshheading:20543867-Female, pubmed-meshheading:20543867-Gene Expression, pubmed-meshheading:20543867-Gene Expression Profiling, pubmed-meshheading:20543867-Gene Expression Regulation, Neoplastic, pubmed-meshheading:20543867-Humans, pubmed-meshheading:20543867-Mesenchymal Stem Cells, pubmed-meshheading:20543867-MicroRNAs, pubmed-meshheading:20543867-Neoplasm Invasiveness, pubmed-meshheading:20543867-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:20543867-Phosphoproteins, pubmed-meshheading:20543867-RNA, Messenger, pubmed-meshheading:20543867-RNA, Small Interfering, pubmed-meshheading:20543867-Transcription Factors, pubmed-meshheading:20543867-Tumor Cells, Cultured, pubmed-meshheading:20543867-Validation Studies as Topic
pubmed:year
2010
pubmed:articleTitle
miR-661 expression in SNAI1-induced epithelial to mesenchymal transition contributes to breast cancer cell invasion by targeting Nectin-1 and StarD10 messengers.
pubmed:affiliation
Cytoskeleton and Cell Plasticity Lab, Life Sciences Research Unit-FSTC, University of Luxembourg, Luxembourg.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't