| pubmed-article:11278365 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11278365 | lifeskim:mentions | umls-concept:C0020792 | lld:lifeskim |
| pubmed-article:11278365 | lifeskim:mentions | umls-concept:C0205145 | lld:lifeskim |
| pubmed-article:11278365 | lifeskim:mentions | umls-concept:C1801960 | lld:lifeskim |
| pubmed-article:11278365 | lifeskim:mentions | umls-concept:C0061817 | lld:lifeskim |
| pubmed-article:11278365 | lifeskim:mentions | umls-concept:C1979853 | lld:lifeskim |
| pubmed-article:11278365 | pubmed:issue | 18 | lld:pubmed |
| pubmed-article:11278365 | pubmed:dateCreated | 2001-4-30 | lld:pubmed |
| pubmed-article:11278365 | pubmed:abstractText | Components of vascular basement membrane are involved in regulating angiogenesis. Recently, tumstatin (the NC1 domain of alpha3 chain of type IV collagen) was identified as possessing anti-angiogenic activity. In the present study, the anti-angiogenic activity of tumstatin was localized to the putative 54-132-amino acid Tum-5 domain, and the activity mediated by alpha(v)beta(3) integrin interaction in an RGD-independent manner. The recombinant Tum-5 produced in Escherichia coli and Pichia Pastoris specifically inhibited proliferation and caused apoptosis of endothelial cells with no significant effect on nonendothelial cells. Tum-5 also inhibited tube formation of endothelial cells on Matrigel and induced G1 endothelial cell cycle arrest. Moreover, anti-angiogenic effect of Tum-5 was also examined in vivo using both a Matrigel plug assay in C57BL/6 mice and human prostate cancer (PC-3) xenografts in nude mice. The in vivo results demonstrate that Tum-5 at 1 mg/kg significantly inhibited growth of PC-3 tumors in association with a decrease in CD31 positive vasculature. These in vivo studies also show that, at molar equivalents, human Tum-5 is at least 10-fold more active than human endostatin. In addition, these studies for the first time suggest that through the action of endogenous inhibitors, alpha(v)beta(3) integrin may also function as a negative regulator of angiogenesis. Taken together, these findings demonstrate that Tum-5, a domain derived from tumstatin, is an effective inhibitor of tumor-associated angiogenesis and a promising candidate for the treatment of cancer. | lld:pubmed |
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| pubmed-article:11278365 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11278365 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11278365 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11278365 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11278365 | pubmed:month | May | lld:pubmed |
| pubmed-article:11278365 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:11278365 | pubmed:author | pubmed-author:ManfrediMM | lld:pubmed |
| pubmed-article:11278365 | pubmed:author | pubmed-author:ReimerCC | lld:pubmed |
| pubmed-article:11278365 | pubmed:author | pubmed-author:MaeshimaYY | lld:pubmed |
| pubmed-article:11278365 | pubmed:author | pubmed-author:KharbandaSS | lld:pubmed |
| pubmed-article:11278365 | pubmed:author | pubmed-author:KalluriRR | lld:pubmed |
| pubmed-article:11278365 | pubmed:author | pubmed-author:HopferHH | lld:pubmed |
| pubmed-article:11278365 | pubmed:author | pubmed-author:HolthausK AKA | lld:pubmed |
| pubmed-article:11278365 | pubmed:author | pubmed-author:ChandamuriB... | lld:pubmed |
| pubmed-article:11278365 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11278365 | pubmed:day | 4 | lld:pubmed |
| pubmed-article:11278365 | pubmed:volume | 276 | lld:pubmed |
| pubmed-article:11278365 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11278365 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11278365 | pubmed:pagination | 15240-8 | lld:pubmed |
| pubmed-article:11278365 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:11278365 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11278365 | pubmed:articleTitle | Identification of the anti-angiogenic site within vascular basement membrane-derived tumstatin. | lld:pubmed |
| pubmed-article:11278365 | pubmed:affiliation | Department of Medicine and the Cancer Center, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA. | lld:pubmed |
| pubmed-article:11278365 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11278365 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:11278365 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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