15-Hydroxyprostaglandin Dehydrogenase Is Down-regulated in Colorectal Cancer
Prostaglandin E2 (PGE2) can stimulate tumor progression by modulating several proneoplastic pathways, including proliferation, angiogenesis, cell migration, invasion, and apoptosis. Although steady-state tissue levels of PGE2 stem from relative rates of biosynthesis and breakdown, most reports exami...
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| Veröffentlicht in: | The Journal of biological chemistry 2005-02, Vol.280 (5), p.3217-3223 |
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| creator | Backlund, Michael G. Mann, Jason R. Holla, Vijaykumar R. Buchanan, F. Gregory Tai, Hsin-Hsiung Musiek, Erik S. Milne, Ginger L. Katkuri, Sharada DuBois, Raymond N. |
| description | Prostaglandin E2 (PGE2) can stimulate tumor progression by modulating several proneoplastic pathways, including proliferation, angiogenesis, cell migration, invasion, and apoptosis. Although steady-state tissue levels of PGE2 stem from relative rates of biosynthesis and breakdown, most reports examining PGE2 have focused solely on the cyclooxygenase-dependent formation of this bioactive lipid. Enzymatic degradation of PGE2 involves the NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH). The present study examined a range of normal tissues in the human and mouse and found high levels of 15-PGDH in the large intestine. By contrast, the expression of 15-PGDH is decreased in several colorectal carcinoma cell lines and in other human malignancies such as breast and lung carcinomas. Consistent with these findings, we observe diminished 15-Pgdh expression in ApcMin+/– mouse adenomas. Enzymatic activity of 15-PGDH correlates with expression levels and the genetic disruption of 15-Pgdh completely blocks production of the urinary PGE2 metabolite. Finally, 15-PGDH expression and activity are significantly down-regulated in human colorectal carcinomas relative to matched normal tissue. In summary, these results suggest a novel tumor suppressive role for 15-PGDH due to loss of expression during colorectal tumor progression. |
| doi_str_mv | 10.1074/jbc.M411221200 |
| format | Article |
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Gregory ; Tai, Hsin-Hsiung ; Musiek, Erik S. ; Milne, Ginger L. ; Katkuri, Sharada ; DuBois, Raymond N.</creator><creatorcontrib>Backlund, Michael G. ; Mann, Jason R. ; Holla, Vijaykumar R. ; Buchanan, F. Gregory ; Tai, Hsin-Hsiung ; Musiek, Erik S. ; Milne, Ginger L. ; Katkuri, Sharada ; DuBois, Raymond N.</creatorcontrib><description>Prostaglandin E2 (PGE2) can stimulate tumor progression by modulating several proneoplastic pathways, including proliferation, angiogenesis, cell migration, invasion, and apoptosis. Although steady-state tissue levels of PGE2 stem from relative rates of biosynthesis and breakdown, most reports examining PGE2 have focused solely on the cyclooxygenase-dependent formation of this bioactive lipid. Enzymatic degradation of PGE2 involves the NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH). The present study examined a range of normal tissues in the human and mouse and found high levels of 15-PGDH in the large intestine. By contrast, the expression of 15-PGDH is decreased in several colorectal carcinoma cell lines and in other human malignancies such as breast and lung carcinomas. Consistent with these findings, we observe diminished 15-Pgdh expression in ApcMin+/– mouse adenomas. Enzymatic activity of 15-PGDH correlates with expression levels and the genetic disruption of 15-Pgdh completely blocks production of the urinary PGE2 metabolite. Finally, 15-PGDH expression and activity are significantly down-regulated in human colorectal carcinomas relative to matched normal tissue. In summary, these results suggest a novel tumor suppressive role for 15-PGDH due to loss of expression during colorectal tumor progression.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.M411221200</identifier><identifier>PMID: 15542609</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Colon - enzymology ; Colorectal Neoplasms - metabolism ; Colorectal Neoplasms - physiopathology ; Cyclooxygenase 2 ; Dinoprostone - metabolism ; Gene Expression Regulation, Enzymologic ; Gene Expression Regulation, Neoplastic ; Humans ; Hydroxyprostaglandin Dehydrogenases - genetics ; Hydroxyprostaglandin Dehydrogenases - metabolism ; Membrane Proteins ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Prostaglandin-Endoperoxide Synthases - metabolism ; Tumor Cells, Cultured</subject><ispartof>The Journal of biological chemistry, 2005-02, Vol.280 (5), p.3217-3223</ispartof><rights>2005 © 2005 ASBMB. 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The present study examined a range of normal tissues in the human and mouse and found high levels of 15-PGDH in the large intestine. By contrast, the expression of 15-PGDH is decreased in several colorectal carcinoma cell lines and in other human malignancies such as breast and lung carcinomas. Consistent with these findings, we observe diminished 15-Pgdh expression in ApcMin+/– mouse adenomas. Enzymatic activity of 15-PGDH correlates with expression levels and the genetic disruption of 15-Pgdh completely blocks production of the urinary PGE2 metabolite. Finally, 15-PGDH expression and activity are significantly down-regulated in human colorectal carcinomas relative to matched normal tissue. In summary, these results suggest a novel tumor suppressive role for 15-PGDH due to loss of expression during colorectal tumor progression.</description><subject>Animals</subject><subject>Colon - enzymology</subject><subject>Colorectal Neoplasms - metabolism</subject><subject>Colorectal Neoplasms - physiopathology</subject><subject>Cyclooxygenase 2</subject><subject>Dinoprostone - metabolism</subject><subject>Gene Expression Regulation, Enzymologic</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Hydroxyprostaglandin Dehydrogenases - genetics</subject><subject>Hydroxyprostaglandin Dehydrogenases - metabolism</subject><subject>Membrane Proteins</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Mutant Strains</subject><subject>Prostaglandin-Endoperoxide Synthases - metabolism</subject><subject>Tumor Cells, Cultured</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1vEzEQxS0EoqHl2mO16oHbhvHXrveCVKVAKwVxoRI3y7Fnd11t1sHepOS_x1EiCgeEL5Y8P795M4-QSwpzCrV4_7iy8y-CUsYoA3hBZhQUL7mk31-SGQCjZcOkOiNvUnqEfERDX5MzKqVgFTQzsqSyvNu7GH7uNzGkyXSDGZ0fi1vsD88djiZhcZ-K2_A0lhG77WAmdEVGFmEIEe1khmJhRovxgrxqzZDw7ek-Jw-fPn5b3JXLr5_vFzfL0opGTqVFxZxsLSjHkBmrGELL0aJxlahYy2vDK44NSJpN2kw2VWU55dAYy4Xg5-TDUXezXa3RWRynaAa9iX5t4l4H4_XfldH3ugs7TZWoK86zwLuTQAw_tpgmvfbJ4pBnx7BNuqpFbq7gvyCtOQgu6wzOj6DNW0wR299uKOhDUjonpZ-Tyh-u_pzhGT9Fk4HrI9D7rn_yEfXKB9vjWjMFWmrO6KGtOkKY173zGHWyHnMWzh-S0S74fxn4BUkQriU</recordid><startdate>20050204</startdate><enddate>20050204</enddate><creator>Backlund, Michael G.</creator><creator>Mann, Jason R.</creator><creator>Holla, Vijaykumar R.</creator><creator>Buchanan, F. 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Gregory</au><au>Tai, Hsin-Hsiung</au><au>Musiek, Erik S.</au><au>Milne, Ginger L.</au><au>Katkuri, Sharada</au><au>DuBois, Raymond N.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>15-Hydroxyprostaglandin Dehydrogenase Is Down-regulated in Colorectal Cancer</atitle><jtitle>The Journal of biological chemistry</jtitle><addtitle>J Biol Chem</addtitle><date>2005-02-04</date><risdate>2005</risdate><volume>280</volume><issue>5</issue><spage>3217</spage><epage>3223</epage><pages>3217-3223</pages><issn>0021-9258</issn><eissn>1083-351X</eissn><abstract>Prostaglandin E2 (PGE2) can stimulate tumor progression by modulating several proneoplastic pathways, including proliferation, angiogenesis, cell migration, invasion, and apoptosis. Although steady-state tissue levels of PGE2 stem from relative rates of biosynthesis and breakdown, most reports examining PGE2 have focused solely on the cyclooxygenase-dependent formation of this bioactive lipid. Enzymatic degradation of PGE2 involves the NAD+-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH). The present study examined a range of normal tissues in the human and mouse and found high levels of 15-PGDH in the large intestine. By contrast, the expression of 15-PGDH is decreased in several colorectal carcinoma cell lines and in other human malignancies such as breast and lung carcinomas. Consistent with these findings, we observe diminished 15-Pgdh expression in ApcMin+/– mouse adenomas. Enzymatic activity of 15-PGDH correlates with expression levels and the genetic disruption of 15-Pgdh completely blocks production of the urinary PGE2 metabolite. Finally, 15-PGDH expression and activity are significantly down-regulated in human colorectal carcinomas relative to matched normal tissue. 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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Animals Colon - enzymology Colorectal Neoplasms - metabolism Colorectal Neoplasms - physiopathology Cyclooxygenase 2 Dinoprostone - metabolism Gene Expression Regulation, Enzymologic Gene Expression Regulation, Neoplastic Humans Hydroxyprostaglandin Dehydrogenases - genetics Hydroxyprostaglandin Dehydrogenases - metabolism Membrane Proteins Mice Mice, Inbred C57BL Mice, Mutant Strains Prostaglandin-Endoperoxide Synthases - metabolism Tumor Cells, Cultured |
| title | 15-Hydroxyprostaglandin Dehydrogenase Is Down-regulated in Colorectal Cancer |
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