| pubmed-article:17721921 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17721921 | lifeskim:mentions | umls-concept:C0346647 | lld:lifeskim |
| pubmed-article:17721921 | lifeskim:mentions | umls-concept:C1947901 | lld:lifeskim |
| pubmed-article:17721921 | lifeskim:mentions | umls-concept:C1706643 | lld:lifeskim |
| pubmed-article:17721921 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:17721921 | pubmed:dateCreated | 2007-11-1 | lld:pubmed |
| pubmed-article:17721921 | pubmed:abstractText | Pancreatic cancer is one of the most aggressive malignant diseases. We recently reported that N-cadherin plays a key role in tumor progression and metastasis in pancreatic cancer. For this study, we sought to determine if an N-cadherin-blocking peptide (ADH-1) could prevent N-cadherin-mediated tumor progression in a mouse model for pancreatic cancer. The effect of ADH-1 on N-cadherin-mediated cell scattering and migration on collagen I was examined using pancreatic cancer cells. We also examined the influence of ADH-1 on cell apoptosis. Furthermore, in vivo animal studies were performed using orthotopic injection of N-cadherin overexpressing BxPC-3 cells with or without ADH-1 treatment. BxPC-3 and Capan-1 cells exhibited increased expression of N-cadherin in response to collagen I. This increase in N-cadherin promoted cell scattering and migration in response to collagen I. ADH-1 prevented these changes, but did not inhibit upregulation of N-cadherin. TUNEL assays and immunoblots for caspase-3 showed that ADH-1 induced apoptosis in a concentration dependent and N-cadherin dependent manner in pancreatic cancer cells. ADH-1 treatment resulted in significant reductions in tumor growth and lung metastasis in a mouse model for pancreatic cancer. The N-cadherin antagonist, ADH-1 has significant antitumor activity against N-cadherin-expressing cells using in vitro assays and in an orthotopic mouse model for pancreatic cancer, raising the possibility that N-cadherin antagonists have therapeutic potential for the treatment of pancreatic cancer in humans. | lld:pubmed |
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| pubmed-article:17721921 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17721921 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17721921 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17721921 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17721921 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:17721921 | pubmed:issn | 1097-0215 | lld:pubmed |
| pubmed-article:17721921 | pubmed:author | pubmed-author:Hollingsworth... | lld:pubmed |
| pubmed-article:17721921 | pubmed:author | pubmed-author:ChaikaNinaN | lld:pubmed |
| pubmed-article:17721921 | pubmed:author | pubmed-author:ShintaniYasus... | lld:pubmed |
| pubmed-article:17721921 | pubmed:author | pubmed-author:JohnsonKeith... | lld:pubmed |
| pubmed-article:17721921 | pubmed:author | pubmed-author:WheelockMarga... | lld:pubmed |
| pubmed-article:17721921 | pubmed:author | pubmed-author:GrandgenettPa... | lld:pubmed |
| pubmed-article:17721921 | pubmed:author | pubmed-author:FukumotoYuriY | lld:pubmed |
| pubmed-article:17721921 | pubmed:copyrightInfo | Copyright 2007 Wiley-Liss, Inc. | lld:pubmed |
| pubmed-article:17721921 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:17721921 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:17721921 | pubmed:volume | 122 | lld:pubmed |
| pubmed-article:17721921 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17721921 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17721921 | pubmed:pagination | 71-7 | lld:pubmed |
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| pubmed-article:17721921 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:17721921 | pubmed:articleTitle | ADH-1 suppresses N-cadherin-dependent pancreatic cancer progression. | lld:pubmed |
| pubmed-article:17721921 | pubmed:affiliation | Department of Oral Biology, University of Nebraska Medical Center, Omaha, NE 68198-7696, USA. | lld:pubmed |
| pubmed-article:17721921 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17721921 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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