Regional differences in prostaglandin E₂ metabolism in human colorectal cancer liver metastases
Prostaglandin (PG) E2 plays a critical role in colorectal cancer (CRC) progression, including epithelial-mesenchymal transition (EMT). Activity of the rate-limiting enzyme for PGE2 catabolism (15-hydroxyprostaglandin dehydrogenase [15-PGDH]) is dependent on availability of NAD+. We tested the hypoth...
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| Veröffentlicht in: | BMC cancer 2013-02, Vol.13 (1), p.92-92, Article 92 |
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| creator | Young, Alastair L Chalmers, Claire R Hawcroft, Gillian Perry, Sarah L Treanor, Darren Toogood, Giles J Jones, Pamela F Hull, Mark A |
| description | Prostaglandin (PG) E2 plays a critical role in colorectal cancer (CRC) progression, including epithelial-mesenchymal transition (EMT). Activity of the rate-limiting enzyme for PGE2 catabolism (15-hydroxyprostaglandin dehydrogenase [15-PGDH]) is dependent on availability of NAD+. We tested the hypothesis that there is intra-tumoral variability in PGE2 content, as well as in levels and activity of 15-PGDH, in human CRC liver metastases (CRCLM). To understand possible underlying mechanisms, we investigated the relationship between hypoxia, 15-PGDH and PGE2 in human CRC cells in vitro.
Tissue from the periphery and centre of 20 human CRCLM was analysed for PGE2 levels, 15-PGDH and cyclooxygenase (COX)-2 expression, 15-PGDH activity, and NAD+/NADH levels. EMT of LIM1863 human CRC cells was induced by transforming growth factor (TGF) β.
PGE2 levels were significantly higher in the centre of CRCLM compared with peripheral tissue (P = 0.04). There were increased levels of 15-PGDH protein in the centre of CRCLM associated with reduced 15-PGDH activity and low NAD+/NADH levels. There was no significant heterogeneity in COX-2 protein expression. NAD+ availability controlled 15-PGDH activity in human CRC cells in vitro. Hypoxia induced 15-PGDH expression in human CRC cells and promoted EMT, in a similar manner to PGE2. Combined 15-PGDH expression and loss of membranous E-cadherin (EMT biomarker) were present in the centre of human CRCLM in vivo.
There is significant intra-tumoral heterogeneity in PGE2 content, 15-PGDH activity and NAD+ availability in human CRCLM. Tumour micro-environment (including hypoxia)-driven differences in PGE2 metabolism should be targeted for novel treatment of advanced CRC. |
| doi_str_mv | 10.1186/1471-2407-13-92 |
| format | Article |
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Tissue from the periphery and centre of 20 human CRCLM was analysed for PGE2 levels, 15-PGDH and cyclooxygenase (COX)-2 expression, 15-PGDH activity, and NAD+/NADH levels. EMT of LIM1863 human CRC cells was induced by transforming growth factor (TGF) β.
PGE2 levels were significantly higher in the centre of CRCLM compared with peripheral tissue (P = 0.04). There were increased levels of 15-PGDH protein in the centre of CRCLM associated with reduced 15-PGDH activity and low NAD+/NADH levels. There was no significant heterogeneity in COX-2 protein expression. NAD+ availability controlled 15-PGDH activity in human CRC cells in vitro. Hypoxia induced 15-PGDH expression in human CRC cells and promoted EMT, in a similar manner to PGE2. Combined 15-PGDH expression and loss of membranous E-cadherin (EMT biomarker) were present in the centre of human CRCLM in vivo.
There is significant intra-tumoral heterogeneity in PGE2 content, 15-PGDH activity and NAD+ availability in human CRCLM. Tumour micro-environment (including hypoxia)-driven differences in PGE2 metabolism should be targeted for novel treatment of advanced CRC.</description><identifier>ISSN: 1471-2407</identifier><identifier>EISSN: 1471-2407</identifier><identifier>DOI: 10.1186/1471-2407-13-92</identifier><identifier>PMID: 23442768</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Binding sites ; Cancer ; Care and treatment ; Cell Hypoxia ; Colorectal cancer ; Colorectal Neoplasms - pathology ; COX-2 inhibitors ; Dinoprostone - metabolism ; Enzymes ; Epithelial-Mesenchymal Transition - drug effects ; Genetic aspects ; Hospitals ; Humans ; Hydroxyprostaglandin Dehydrogenases - metabolism ; Hypotheses ; Hypoxia ; Immunohistochemistry ; Liver ; Liver Neoplasms - metabolism ; Liver Neoplasms - secondary ; Medical research ; Metabolism ; Metastasis ; Methods ; Microarray Analysis ; Neoplasm Proteins - metabolism ; Physiological aspects ; Prostaglandins E ; Proteins ; Stem cells ; Transforming Growth Factor beta - pharmacology ; Transforming growth factors ; Tumor Cells, Cultured ; Tumor Microenvironment ; Tumors</subject><ispartof>BMC cancer, 2013-02, Vol.13 (1), p.92-92, Article 92</ispartof><rights>COPYRIGHT 2013 BioMed Central Ltd.</rights><rights>2013 Young et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright ©2013 Young et al; licensee BioMed Central Ltd. 2013 Young et al; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b5272-a7c172e0aff25ebcf5e6207c2b01ca31c77533db31f779f279e2ff83590761b53</citedby><cites>FETCH-LOGICAL-b5272-a7c172e0aff25ebcf5e6207c2b01ca31c77533db31f779f279e2ff83590761b53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3598740/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3598740/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23442768$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Young, Alastair L</creatorcontrib><creatorcontrib>Chalmers, Claire R</creatorcontrib><creatorcontrib>Hawcroft, Gillian</creatorcontrib><creatorcontrib>Perry, Sarah L</creatorcontrib><creatorcontrib>Treanor, Darren</creatorcontrib><creatorcontrib>Toogood, Giles J</creatorcontrib><creatorcontrib>Jones, Pamela F</creatorcontrib><creatorcontrib>Hull, Mark A</creatorcontrib><title>Regional differences in prostaglandin E₂ metabolism in human colorectal cancer liver metastases</title><title>BMC cancer</title><addtitle>BMC Cancer</addtitle><description>Prostaglandin (PG) E2 plays a critical role in colorectal cancer (CRC) progression, including epithelial-mesenchymal transition (EMT). Activity of the rate-limiting enzyme for PGE2 catabolism (15-hydroxyprostaglandin dehydrogenase [15-PGDH]) is dependent on availability of NAD+. We tested the hypothesis that there is intra-tumoral variability in PGE2 content, as well as in levels and activity of 15-PGDH, in human CRC liver metastases (CRCLM). To understand possible underlying mechanisms, we investigated the relationship between hypoxia, 15-PGDH and PGE2 in human CRC cells in vitro.
Tissue from the periphery and centre of 20 human CRCLM was analysed for PGE2 levels, 15-PGDH and cyclooxygenase (COX)-2 expression, 15-PGDH activity, and NAD+/NADH levels. EMT of LIM1863 human CRC cells was induced by transforming growth factor (TGF) β.
PGE2 levels were significantly higher in the centre of CRCLM compared with peripheral tissue (P = 0.04). There were increased levels of 15-PGDH protein in the centre of CRCLM associated with reduced 15-PGDH activity and low NAD+/NADH levels. There was no significant heterogeneity in COX-2 protein expression. NAD+ availability controlled 15-PGDH activity in human CRC cells in vitro. Hypoxia induced 15-PGDH expression in human CRC cells and promoted EMT, in a similar manner to PGE2. Combined 15-PGDH expression and loss of membranous E-cadherin (EMT biomarker) were present in the centre of human CRCLM in vivo.
There is significant intra-tumoral heterogeneity in PGE2 content, 15-PGDH activity and NAD+ availability in human CRCLM. Tumour micro-environment (including hypoxia)-driven differences in PGE2 metabolism should be targeted for novel treatment of advanced CRC.</description><subject>Binding sites</subject><subject>Cancer</subject><subject>Care and treatment</subject><subject>Cell Hypoxia</subject><subject>Colorectal cancer</subject><subject>Colorectal Neoplasms - pathology</subject><subject>COX-2 inhibitors</subject><subject>Dinoprostone - metabolism</subject><subject>Enzymes</subject><subject>Epithelial-Mesenchymal Transition - drug effects</subject><subject>Genetic aspects</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Hydroxyprostaglandin Dehydrogenases - metabolism</subject><subject>Hypotheses</subject><subject>Hypoxia</subject><subject>Immunohistochemistry</subject><subject>Liver</subject><subject>Liver Neoplasms - metabolism</subject><subject>Liver Neoplasms - secondary</subject><subject>Medical research</subject><subject>Metabolism</subject><subject>Metastasis</subject><subject>Methods</subject><subject>Microarray Analysis</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Physiological aspects</subject><subject>Prostaglandins E</subject><subject>Proteins</subject><subject>Stem cells</subject><subject>Transforming Growth Factor beta - pharmacology</subject><subject>Transforming growth factors</subject><subject>Tumor Cells, Cultured</subject><subject>Tumor Microenvironment</subject><subject>Tumors</subject><issn>1471-2407</issn><issn>1471-2407</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNp1kt9r1TAUx4sobk6ffZOCIO6hW360TfsizDF1MBhMfQ5petKbkTbXpB36uj_Vv8TT3Xl3K5NAfn7ON8n3nCR5TckRpVV5THNBM5YTkVGe1exJsr_deboz30texHhNCBUVqZ4ne4znORNltZ-oK-isH5RLW2sMBBg0xNQO6Tr4OKrOqaHF1dnv29u0h1E13tnYz8Bq6tWQau98AD2igFYYG1Jnb7CfWYyPEF8mz4xyEV7djwfJ909n306_ZBeXn89PTy6ypmCCZUpoKhgQZQwroNGmgJIRoVlDqFacaiEKztuGUyNEbZiogRlT8aImoqRNwQ-SDxvd9dT00GoYxqCcXAfbq_BLemXl8mSwK9n5G4kSlcgJCnzcCDTW_0dgeaJ9L2eL5WyxpFzWDEXe378i-B8TxFH2Nmpw6CP4KSKFOShoQXNE3_6DXvspYCruqLxihNfkgeqUA2kH4_FuPYvKk4LnJalKNn_-6BEKWwu91X4AY3F_EXC4CEBmhJ9jp6YY5fnXqyX7boddgXLjKno3jVg4cQkeb0CNxRMDmK15lMi5Xh-x681u0rb83wLlfwAU0uS2</recordid><startdate>20130226</startdate><enddate>20130226</enddate><creator>Young, Alastair L</creator><creator>Chalmers, Claire R</creator><creator>Hawcroft, Gillian</creator><creator>Perry, Sarah L</creator><creator>Treanor, Darren</creator><creator>Toogood, Giles J</creator><creator>Jones, Pamela F</creator><creator>Hull, Mark A</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>ISR</scope><scope>3V.</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20130226</creationdate><title>Regional differences in prostaglandin E₂ metabolism in human colorectal cancer liver metastases</title><author>Young, Alastair L ; Chalmers, Claire R ; Hawcroft, Gillian ; Perry, Sarah L ; Treanor, Darren ; Toogood, Giles J ; Jones, Pamela F ; Hull, Mark A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b5272-a7c172e0aff25ebcf5e6207c2b01ca31c77533db31f779f279e2ff83590761b53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Binding sites</topic><topic>Cancer</topic><topic>Care and treatment</topic><topic>Cell Hypoxia</topic><topic>Colorectal cancer</topic><topic>Colorectal Neoplasms - pathology</topic><topic>COX-2 inhibitors</topic><topic>Dinoprostone - metabolism</topic><topic>Enzymes</topic><topic>Epithelial-Mesenchymal Transition - drug effects</topic><topic>Genetic aspects</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Hydroxyprostaglandin Dehydrogenases - metabolism</topic><topic>Hypotheses</topic><topic>Hypoxia</topic><topic>Immunohistochemistry</topic><topic>Liver</topic><topic>Liver Neoplasms - metabolism</topic><topic>Liver Neoplasms - secondary</topic><topic>Medical research</topic><topic>Metabolism</topic><topic>Metastasis</topic><topic>Methods</topic><topic>Microarray Analysis</topic><topic>Neoplasm Proteins - metabolism</topic><topic>Physiological aspects</topic><topic>Prostaglandins E</topic><topic>Proteins</topic><topic>Stem cells</topic><topic>Transforming Growth Factor beta - pharmacology</topic><topic>Transforming growth factors</topic><topic>Tumor Cells, Cultured</topic><topic>Tumor Microenvironment</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Young, Alastair L</creatorcontrib><creatorcontrib>Chalmers, Claire R</creatorcontrib><creatorcontrib>Hawcroft, Gillian</creatorcontrib><creatorcontrib>Perry, Sarah L</creatorcontrib><creatorcontrib>Treanor, Darren</creatorcontrib><creatorcontrib>Toogood, Giles J</creatorcontrib><creatorcontrib>Jones, Pamela F</creatorcontrib><creatorcontrib>Hull, Mark A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BMC cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Young, Alastair L</au><au>Chalmers, Claire R</au><au>Hawcroft, Gillian</au><au>Perry, Sarah L</au><au>Treanor, Darren</au><au>Toogood, Giles J</au><au>Jones, Pamela F</au><au>Hull, Mark A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regional differences in prostaglandin E₂ metabolism in human colorectal cancer liver metastases</atitle><jtitle>BMC cancer</jtitle><addtitle>BMC Cancer</addtitle><date>2013-02-26</date><risdate>2013</risdate><volume>13</volume><issue>1</issue><spage>92</spage><epage>92</epage><pages>92-92</pages><artnum>92</artnum><issn>1471-2407</issn><eissn>1471-2407</eissn><abstract>Prostaglandin (PG) E2 plays a critical role in colorectal cancer (CRC) progression, including epithelial-mesenchymal transition (EMT). Activity of the rate-limiting enzyme for PGE2 catabolism (15-hydroxyprostaglandin dehydrogenase [15-PGDH]) is dependent on availability of NAD+. We tested the hypothesis that there is intra-tumoral variability in PGE2 content, as well as in levels and activity of 15-PGDH, in human CRC liver metastases (CRCLM). To understand possible underlying mechanisms, we investigated the relationship between hypoxia, 15-PGDH and PGE2 in human CRC cells in vitro.
Tissue from the periphery and centre of 20 human CRCLM was analysed for PGE2 levels, 15-PGDH and cyclooxygenase (COX)-2 expression, 15-PGDH activity, and NAD+/NADH levels. EMT of LIM1863 human CRC cells was induced by transforming growth factor (TGF) β.
PGE2 levels were significantly higher in the centre of CRCLM compared with peripheral tissue (P = 0.04). There were increased levels of 15-PGDH protein in the centre of CRCLM associated with reduced 15-PGDH activity and low NAD+/NADH levels. There was no significant heterogeneity in COX-2 protein expression. NAD+ availability controlled 15-PGDH activity in human CRC cells in vitro. Hypoxia induced 15-PGDH expression in human CRC cells and promoted EMT, in a similar manner to PGE2. Combined 15-PGDH expression and loss of membranous E-cadherin (EMT biomarker) were present in the centre of human CRCLM in vivo.
There is significant intra-tumoral heterogeneity in PGE2 content, 15-PGDH activity and NAD+ availability in human CRCLM. Tumour micro-environment (including hypoxia)-driven differences in PGE2 metabolism should be targeted for novel treatment of advanced CRC.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>23442768</pmid><doi>10.1186/1471-2407-13-92</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Binding sites Cancer Care and treatment Cell Hypoxia Colorectal cancer Colorectal Neoplasms - pathology COX-2 inhibitors Dinoprostone - metabolism Enzymes Epithelial-Mesenchymal Transition - drug effects Genetic aspects Hospitals Humans Hydroxyprostaglandin Dehydrogenases - metabolism Hypotheses Hypoxia Immunohistochemistry Liver Liver Neoplasms - metabolism Liver Neoplasms - secondary Medical research Metabolism Metastasis Methods Microarray Analysis Neoplasm Proteins - metabolism Physiological aspects Prostaglandins E Proteins Stem cells Transforming Growth Factor beta - pharmacology Transforming growth factors Tumor Cells, Cultured Tumor Microenvironment Tumors |
| title | Regional differences in prostaglandin E₂ metabolism in human colorectal cancer liver metastases |
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