| pubmed-article:19286570 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19286570 | lifeskim:mentions | umls-concept:C0376358 | lld:lifeskim |
| pubmed-article:19286570 | lifeskim:mentions | umls-concept:C0245382 | lld:lifeskim |
| pubmed-article:19286570 | lifeskim:mentions | umls-concept:C1947901 | lld:lifeskim |
| pubmed-article:19286570 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:19286570 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:19286570 | pubmed:dateCreated | 2009-4-3 | lld:pubmed |
| pubmed-article:19286570 | pubmed:abstractText | Galectin-3, a beta-galactoside-binding protein, has been implicated in a variety of biological functions including cell proliferation, apoptosis, angiogenesis, tumor progression, and metastasis. The present study was undertaken to understand the role of galectin-3 in the progression of prostate cancer. Immunohistochemical analysis of galectin-3 expression revealed that galectin-3 was cleaved during the progression of prostate cancer. Galectin-3 knockdown by small interfering RNA (siRNA) was associated with reduced cell migration, invasion, cell proliferation, anchorage-independent colony formation, and tumor growth in the prostates of nude mice. Galectin-3 knockdown in human prostate cancer PC3 cells led to cell-cycle arrest at G(1) phase, up-regulation of nuclear p21, and hypophosphorylation of the retinoblastoma tumor suppressor protein (pRb), with no effect on cyclin D1, cyclin E, cyclin-dependent kinases (CDK2 and CDK4), and p27 protein expression levels. The data obtained here implicate galectin-3 in prostate cancer progression and suggest that galectin-3 may serve as both a diagnostic marker and therapeutic target for future disease treatments. | lld:pubmed |
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| pubmed-article:19286570 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19286570 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19286570 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:19286570 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19286570 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:19286570 | pubmed:issn | 1525-2191 | lld:pubmed |
| pubmed-article:19286570 | pubmed:author | pubmed-author:RazAvrahamA | lld:pubmed |
| pubmed-article:19286570 | pubmed:author | pubmed-author:WangYiY | lld:pubmed |
| pubmed-article:19286570 | pubmed:author | pubmed-author:PientaKenneth... | lld:pubmed |
| pubmed-article:19286570 | pubmed:author | pubmed-author:Nangia-Makker... | lld:pubmed |
| pubmed-article:19286570 | pubmed:author | pubmed-author:HoganVictorV | lld:pubmed |
| pubmed-article:19286570 | pubmed:author | pubmed-author:TaitLarryL | lld:pubmed |
| pubmed-article:19286570 | pubmed:author | pubmed-author:BalanVitalyV | lld:pubmed |
| pubmed-article:19286570 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19286570 | pubmed:volume | 174 | lld:pubmed |
| pubmed-article:19286570 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19286570 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19286570 | pubmed:pagination | 1515-23 | lld:pubmed |
| pubmed-article:19286570 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:19286570 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19286570 | pubmed:articleTitle | Regulation of prostate cancer progression by galectin-3. | lld:pubmed |
| pubmed-article:19286570 | pubmed:affiliation | Tumor Progression and Metastasis, Karmanos Cancer Institute, School of Medicine, Wayne State University, 110 East Warren Ave., Detroit, MI 48201, USA. | lld:pubmed |
| pubmed-article:19286570 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19286570 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:19286570 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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