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DC Field | Value | Language |
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dc.creator | Nibedita Gupta | - |
dc.creator | Fee Schmitt | - |
dc.creator | Sina Grebhardt | - |
dc.creator | Doris Mayer | - |
dc.date | 2011 | - |
dc.date.accessioned | 2013-05-30T13:10:42Z | - |
dc.date.available | 2013-05-30T13:10:42Z | - |
dc.date.issued | 2013-05-30 | - |
dc.identifier | http://www.mdpi.com/2072-6694/3/3/2990/ | - |
dc.identifier | http://www.doaj.org/doaj?func=openurl&genre=article&issn=20726694&date=2011&volume=3&issue=3&spage=2990 | - |
dc.identifier.uri | http://koha.mediu.edu.my:8181/jspui/handle/123456789/5642 | - |
dc.description | Estrogen receptor-alpha (ERα) is a key factor in the development of breast cancer in humans. The expression and activity of ERα is regulated by a multitude of intracellular and extracellular signals. Here we show a cross-talk between β-catenin and ERα in human breast cancer cells. Knockdown of β-catenin by RNAi resulted in significant reduction of ERα mRNA and/or protein levels in MCF-7, T-47D, and BT-474 breast cancer cells and in significant reduction of estradiol-induced expression of the ERα target genes pS2 and GREB1. In addition β-catenin silencing resulted in significant decrease of growth of MCF-7 cells both in the absence and presence of estradiol. β-catenin and ERα could not be co-immunoprecipitated by ERα antibodies from lysates of E2-treated or untreated cells suggesting lack of direct physical interaction. It is concluded that β-catenin is a positive regulator of ERα mRNA and protein expression. | - |
dc.language | eng | - |
dc.publisher | Molecular Diversity Preservation International | - |
dc.source | Cancers | - |
dc.subject | β-catenin | - |
dc.subject | estrogen receptor | - |
dc.subject | cross-talk | - |
dc.subject | gene expression | - |
dc.subject | transcriptional activity | - |
dc.subject | breast cancer cell | - |
dc.title | β-Catenin Is a Positive Regulator of Estrogen Receptor-α Function in Breast Cancer Cells | - |
Appears in Collections: | Health Sciences |
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