Linked Life Data

20817789

Source:http://linkedlifedata.com/resource/pubmed/id/20817789

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2010-11-1
pubmed:abstractText
The orphan nuclear receptor liver receptor homologue-1 (LRH-1) has roles in the development, cholesterol and bile acid homeostasis, and steroidogenesis. It also enhances proliferation and cell cycle progression of cancer cells. In breast cancer, LRH-1 expression is associated with invasive breast cancer; positively correlates with ER? status and aromatase activity; and promotes oestrogen-dependent cell proliferation. However, the mechanism of action of LRH-1 in breast cancer epithelial cells is still not clear. By silencing or over-expressing LRH-1 in ER-positive MCF-7 and ER-negative MDA-MB-231 breast cancer cells, we have demonstrated that LRH-1 promotes motility and cell invasiveness. Similar effects were observed in the non-tumourigenic mammary epithelial cell line, MCF-10A. Remodelling of the actin cytoskeleton and E-cadherin cleavage was observed with LRH-1 over-expression, contributing to increased migratory and invasive properties. Additionally, in LRH-1 over-expressing cells, the truncation of the 120?kDa E-cadherin to the inactive 97?kDa form was observed. These post-translational modifications in E-cadherin may be associated with LRH-1-dependent changes to matrix metalloproteinase 9 expression. These findings suggest a new role of LRH-1 in promoting migration and invasion in breast cancer, independent of oestrogen sensitivity. Therefore, LRH-1 may represent a new target for breast cancer therapeutics.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1479-6821
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
965-75
pubmed:dateRevised
2011-4-20
pubmed:meshHeading
pubmed-meshheading:20817789-Analysis of Variance, pubmed-meshheading:20817789-Blotting, Western, pubmed-meshheading:20817789-Breast Neoplasms, pubmed-meshheading:20817789-Cadherins, pubmed-meshheading:20817789-Cell Count, pubmed-meshheading:20817789-Cell Line, Tumor, pubmed-meshheading:20817789-Cell Movement, pubmed-meshheading:20817789-Cell Proliferation, pubmed-meshheading:20817789-Cytoskeleton, pubmed-meshheading:20817789-Estrogen Receptor alpha, pubmed-meshheading:20817789-Female, pubmed-meshheading:20817789-Humans, pubmed-meshheading:20817789-Matrix Metalloproteinase 9, pubmed-meshheading:20817789-Neoplasm Invasiveness, pubmed-meshheading:20817789-Protein Processing, Post-Translational, pubmed-meshheading:20817789-Receptors, Cytoplasmic and Nuclear, pubmed-meshheading:20817789-Transfection
pubmed:year
2010
pubmed:articleTitle
The orphan nuclear receptor LRH-1 promotes breast cancer motility and invasion.
pubmed:affiliation
Cancer Drug Discovery Laboratory, Prince Henry's Institute, 246 Clayton Road, Melbourne, Victoria 3168, Australia. ashwini.chand@princehenrys.org
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't