| pubmed-article:9261162 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9261162 | lifeskim:mentions | umls-concept:C0389003 | lld:lifeskim |
| pubmed-article:9261162 | lifeskim:mentions | umls-concept:C0225336 | lld:lifeskim |
| pubmed-article:9261162 | lifeskim:mentions | umls-concept:C1510411 | lld:lifeskim |
| pubmed-article:9261162 | lifeskim:mentions | umls-concept:C1514559 | lld:lifeskim |
| pubmed-article:9261162 | lifeskim:mentions | umls-concept:C2826170 | lld:lifeskim |
| pubmed-article:9261162 | pubmed:issue | 34 | lld:pubmed |
| pubmed-article:9261162 | pubmed:dateCreated | 1997-9-15 | lld:pubmed |
| pubmed-article:9261162 | pubmed:abstractText | The cyclooxygenase (Cox) enzyme catalyzes the rate-limiting oxidative and peroxidative enzymatic steps in the biosynthesis of prostanoids. Both Cox-1 and -2 genes encode the two isoenzymes that carry out similar enzymatic steps. Enhanced Cox activity is associated with proliferative diseases such as colon cancer. To determine if a cause and effect relationship exists between Cox isoenzyme overexpression and tumorigenesis, the human Cox-1 and Cox-2 isoenzymes were transfected into ECV immortalized endothelial cells. Although numerous clones of Cox-1 expressing cells were obtained, Cox-2 overexpression resulted in growth disadvantage and increased cell death. In contrast, Cox-1 overexpressing cells expressed high levels of the functional Cox-1 polypeptide in the endoplasmic reticulum and the nucleus. In vitro proliferation of these cells was reduced compared with vector-transfected ECV cells. Cox-1 overexpression also enhanced the tumor necrosis factor-alpha-induced apoptosis of ECV cells 2-fold. In contrast to the in vitro behavior, ECV-Cox-1 cells proliferated aggressively and formed tumors in athymic "nude" mice, whereas the vector-transfected counterparts did not. The growth of Cox-1-induced tumors was not inhibited by indomethacin, suggesting a nonprostanoid function of Cox-1. ECV-Cox-1-derived tumors were angiosarcoma-like and contained numerous host-derived neovessels. These data suggest that Cox-1 overexpression in immortalized ECV endothelial cells results in nuclear localization of the polypeptide and tumorigenesis. | lld:pubmed |
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| pubmed-article:9261162 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:9261162 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9261162 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9261162 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:9261162 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:9261162 | pubmed:author | pubmed-author:SmithEE | lld:pubmed |
| pubmed-article:9261162 | pubmed:author | pubmed-author:LiH LHL | lld:pubmed |
| pubmed-article:9261162 | pubmed:author | pubmed-author:HaudenschildC... | lld:pubmed |
| pubmed-article:9261162 | pubmed:author | pubmed-author:RistimäkiAA | lld:pubmed |
| pubmed-article:9261162 | pubmed:author | pubmed-author:MacPheeMM | lld:pubmed |
| pubmed-article:9261162 | pubmed:author | pubmed-author:NarkoKK | lld:pubmed |
| pubmed-article:9261162 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9261162 | pubmed:day | 22 | lld:pubmed |
| pubmed-article:9261162 | pubmed:volume | 272 | lld:pubmed |
| pubmed-article:9261162 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9261162 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9261162 | pubmed:pagination | 21455-60 | lld:pubmed |
| pubmed-article:9261162 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:9261162 | pubmed:year | 1997 | lld:pubmed |
| pubmed-article:9261162 | pubmed:articleTitle | Tumorigenic transformation of immortalized ECV endothelial cells by cyclooxygenase-1 overexpression. | lld:pubmed |
| pubmed-article:9261162 | pubmed:affiliation | Department of Clinical Chemistry and Obstetrics and Gynecology, Haartman Institute, Helsinki University, Helsinki, Finland. | lld:pubmed |
| pubmed-article:9261162 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9261162 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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