Overexpression of VEGF121, but not VEGF165 or FGF-1, improves oxygenation in MCF-7 breast tumours
Vascular endothelial growth factor (VEGF) is an intensively studied molecule that has significant potential, both in stimulating angiogenesis and as a target for antiangiogenic approaches. We utilised MCF-7 breast cancer cells transfected with either of two of the major VEGF isoforms, VEGF 121 or VE...
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| Veröffentlicht in: | British journal of cancer 2004-01, Vol.90 (2), p.430-435 |
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| creator | Fenton, B M Paoni, S F Liu, W Cheng, S-Y Hu, B Ding, I |
| description | Vascular endothelial growth factor (VEGF) is an intensively studied molecule that has significant potential, both in stimulating angiogenesis and as a target for antiangiogenic approaches. We utilised MCF-7 breast cancer cells transfected with either of two of the major VEGF isoforms, VEGF
121
or VEGF
165
, or fibroblast growth factor-1 (FGF-1) to distinguish the effects of these factors on tumour growth, vascular function, and oxygen delivery. While each transfectant demonstrated substantially increased tumorigenicity and growth rate compared to vector controls, only VEGF
121
produced a combination of significantly reduced total and perfused vessel spacing, as well as a corresponding reduction in overall tumour hypoxia. Such pathophysiological effects are of potential importance, since antiangiogenic agents designed to block VEGF isoforms could in turn result in the development of therapeutically unfavourable environments. If antiangiogenic agents are also combined with conventional therapies such as irradiation or chemotherapy, microregional deficiencies in oxygenation could play a key role in ultimate therapeutic success. |
| doi_str_mv | 10.1038/sj.bjc.6601539 |
| format | Article |
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121
or VEGF
165
, or fibroblast growth factor-1 (FGF-1) to distinguish the effects of these factors on tumour growth, vascular function, and oxygen delivery. While each transfectant demonstrated substantially increased tumorigenicity and growth rate compared to vector controls, only VEGF
121
produced a combination of significantly reduced total and perfused vessel spacing, as well as a corresponding reduction in overall tumour hypoxia. Such pathophysiological effects are of potential importance, since antiangiogenic agents designed to block VEGF isoforms could in turn result in the development of therapeutically unfavourable environments. If antiangiogenic agents are also combined with conventional therapies such as irradiation or chemotherapy, microregional deficiencies in oxygenation could play a key role in ultimate therapeutic success.</description><identifier>ISSN: 0007-0920</identifier><identifier>EISSN: 1532-1827</identifier><identifier>DOI: 10.1038/sj.bjc.6601539</identifier><identifier>PMID: 14735189</identifier><identifier>CODEN: BJCAAI</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Angiogenesis ; Angiogenesis Inhibitors - therapeutic use ; Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Breast cancer ; Breast Neoplasms - pathology ; Cancer Research ; Cancer therapies ; Chemotherapy ; Drug Resistance ; Epidemiology ; Female ; Fibroblast Growth Factor 1 - biosynthesis ; Fibroblast Growth Factor 1 - pharmacology ; Gene Expression Regulation, Neoplastic ; Humans ; Hypoxia ; Medical research ; Medical sciences ; Molecular and Cellular Pathology ; Molecular Medicine ; Neovascularization, Pathologic ; Oncology ; Oxygen - metabolism ; Transfection ; Tumor Cells, Cultured ; Tumors ; Vascular endothelial growth factor ; Vascular Endothelial Growth Factor A - biosynthesis ; Vascular Endothelial Growth Factor A - pharmacology</subject><ispartof>British journal of cancer, 2004-01, Vol.90 (2), p.430-435</ispartof><rights>The Author(s) 2004</rights><rights>2004 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jan 26, 2004</rights><rights>Copyright © 2004 Cancer Research UK 2004 Cancer Research UK</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3989-a02372d7358edb9f933034bc782c34576b2b0b688b79afd51e67e30395a337403</citedby><cites>FETCH-LOGICAL-c3989-a02372d7358edb9f933034bc782c34576b2b0b688b79afd51e67e30395a337403</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/PMC2409569/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2409569/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15678380$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14735189$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fenton, B M</creatorcontrib><creatorcontrib>Paoni, S F</creatorcontrib><creatorcontrib>Liu, W</creatorcontrib><creatorcontrib>Cheng, S-Y</creatorcontrib><creatorcontrib>Hu, B</creatorcontrib><creatorcontrib>Ding, I</creatorcontrib><title>Overexpression of VEGF121, but not VEGF165 or FGF-1, improves oxygenation in MCF-7 breast tumours</title><title>British journal of cancer</title><addtitle>Br J Cancer</addtitle><addtitle>Br J Cancer</addtitle><description>Vascular endothelial growth factor (VEGF) is an intensively studied molecule that has significant potential, both in stimulating angiogenesis and as a target for antiangiogenic approaches. We utilised MCF-7 breast cancer cells transfected with either of two of the major VEGF isoforms, VEGF
121
or VEGF
165
, or fibroblast growth factor-1 (FGF-1) to distinguish the effects of these factors on tumour growth, vascular function, and oxygen delivery. While each transfectant demonstrated substantially increased tumorigenicity and growth rate compared to vector controls, only VEGF
121
produced a combination of significantly reduced total and perfused vessel spacing, as well as a corresponding reduction in overall tumour hypoxia. Such pathophysiological effects are of potential importance, since antiangiogenic agents designed to block VEGF isoforms could in turn result in the development of therapeutically unfavourable environments. If antiangiogenic agents are also combined with conventional therapies such as irradiation or chemotherapy, microregional deficiencies in oxygenation could play a key role in ultimate therapeutic success.</description><subject>Angiogenesis</subject><subject>Angiogenesis Inhibitors - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - pathology</subject><subject>Cancer Research</subject><subject>Cancer therapies</subject><subject>Chemotherapy</subject><subject>Drug Resistance</subject><subject>Epidemiology</subject><subject>Female</subject><subject>Fibroblast Growth Factor 1 - biosynthesis</subject><subject>Fibroblast Growth Factor 1 - pharmacology</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Medical research</subject><subject>Medical sciences</subject><subject>Molecular and Cellular Pathology</subject><subject>Molecular Medicine</subject><subject>Neovascularization, Pathologic</subject><subject>Oncology</subject><subject>Oxygen - metabolism</subject><subject>Transfection</subject><subject>Tumor Cells, Cultured</subject><subject>Tumors</subject><subject>Vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - biosynthesis</subject><subject>Vascular Endothelial Growth Factor A - pharmacology</subject><issn>0007-0920</issn><issn>1532-1827</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kU1r3DAQhkVpaDZprz0WUWhP9UYfliVdAmWJt4GEXNpehaSVtza2tJXsJfn31bIm2xZyGqR5ZuadeQF4j9ESIyquUrc0nV1WFcKMyldgkQMpsCD8NVgghHiBJEHn4CKlLj8lEvwNOMclpwwLuQD6Ye-ie9xFl1IbPAwN_HmzrjHBX6CZRujDePyoGAwR1uu6yJl22MWwdwmGx6et83o8lLYe3q_qgkMTnU4jHKchTDG9BWeN7pN7N8dL8KO--b76Vtw9rG9XX-8KS6WQhUaEcrLJuoTbGNlIShEtjeWCWFoyXhlikKmEMFzqZsOwq7jLiGSaUl4iegmuj313kxncxjo_Rt2rXWwHHZ9U0K36N-PbX2ob9oqUSLJK5gaf5wYx_J5cGtXQJuv6XnsXpqQEwvkKjGfw439glxf1eTlFiJSCM1lmaHmEbAwpRdc8K8FIHaxTqVPZOjVblws-_K3_hM9eZeDTDOhkdd9E7W2bThyruKDicIirI5dyym9dPMl7YfQfvSOvJw</recordid><startdate>20040126</startdate><enddate>20040126</enddate><creator>Fenton, B M</creator><creator>Paoni, S F</creator><creator>Liu, W</creator><creator>Cheng, S-Y</creator><creator>Hu, B</creator><creator>Ding, I</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>IQODW</scope><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>3V.</scope><scope>7RV</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20040126</creationdate><title>Overexpression of VEGF121, but not VEGF165 or FGF-1, improves oxygenation in MCF-7 breast tumours</title><author>Fenton, B M ; Paoni, S F ; Liu, W ; Cheng, S-Y ; Hu, B ; Ding, I</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3989-a02372d7358edb9f933034bc782c34576b2b0b688b79afd51e67e30395a337403</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Angiogenesis</topic><topic>Angiogenesis Inhibitors - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - pathology</topic><topic>Cancer Research</topic><topic>Cancer therapies</topic><topic>Chemotherapy</topic><topic>Drug Resistance</topic><topic>Epidemiology</topic><topic>Female</topic><topic>Fibroblast Growth Factor 1 - biosynthesis</topic><topic>Fibroblast Growth Factor 1 - pharmacology</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Hypoxia</topic><topic>Medical research</topic><topic>Medical sciences</topic><topic>Molecular and Cellular Pathology</topic><topic>Molecular Medicine</topic><topic>Neovascularization, Pathologic</topic><topic>Oncology</topic><topic>Oxygen - metabolism</topic><topic>Transfection</topic><topic>Tumor Cells, Cultured</topic><topic>Tumors</topic><topic>Vascular endothelial growth factor</topic><topic>Vascular Endothelial Growth Factor A - biosynthesis</topic><topic>Vascular Endothelial Growth Factor A - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fenton, B M</creatorcontrib><creatorcontrib>Paoni, S F</creatorcontrib><creatorcontrib>Liu, W</creatorcontrib><creatorcontrib>Cheng, S-Y</creatorcontrib><creatorcontrib>Hu, B</creatorcontrib><creatorcontrib>Ding, I</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</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>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</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>British journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fenton, B M</au><au>Paoni, S F</au><au>Liu, W</au><au>Cheng, S-Y</au><au>Hu, B</au><au>Ding, I</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Overexpression of VEGF121, but not VEGF165 or FGF-1, improves oxygenation in MCF-7 breast tumours</atitle><jtitle>British journal of cancer</jtitle><stitle>Br J Cancer</stitle><addtitle>Br J Cancer</addtitle><date>2004-01-26</date><risdate>2004</risdate><volume>90</volume><issue>2</issue><spage>430</spage><epage>435</epage><pages>430-435</pages><issn>0007-0920</issn><eissn>1532-1827</eissn><coden>BJCAAI</coden><abstract>Vascular endothelial growth factor (VEGF) is an intensively studied molecule that has significant potential, both in stimulating angiogenesis and as a target for antiangiogenic approaches. We utilised MCF-7 breast cancer cells transfected with either of two of the major VEGF isoforms, VEGF
121
or VEGF
165
, or fibroblast growth factor-1 (FGF-1) to distinguish the effects of these factors on tumour growth, vascular function, and oxygen delivery. While each transfectant demonstrated substantially increased tumorigenicity and growth rate compared to vector controls, only VEGF
121
produced a combination of significantly reduced total and perfused vessel spacing, as well as a corresponding reduction in overall tumour hypoxia. Such pathophysiological effects are of potential importance, since antiangiogenic agents designed to block VEGF isoforms could in turn result in the development of therapeutically unfavourable environments. If antiangiogenic agents are also combined with conventional therapies such as irradiation or chemotherapy, microregional deficiencies in oxygenation could play a key role in ultimate therapeutic success.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>14735189</pmid><doi>10.1038/sj.bjc.6601539</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Angiogenesis Angiogenesis Inhibitors - therapeutic use Biological and medical sciences Biomedical and Life Sciences Biomedicine Breast cancer Breast Neoplasms - pathology Cancer Research Cancer therapies Chemotherapy Drug Resistance Epidemiology Female Fibroblast Growth Factor 1 - biosynthesis Fibroblast Growth Factor 1 - pharmacology Gene Expression Regulation, Neoplastic Humans Hypoxia Medical research Medical sciences Molecular and Cellular Pathology Molecular Medicine Neovascularization, Pathologic Oncology Oxygen - metabolism Transfection Tumor Cells, Cultured Tumors Vascular endothelial growth factor Vascular Endothelial Growth Factor A - biosynthesis Vascular Endothelial Growth Factor A - pharmacology |
| title | Overexpression of VEGF121, but not VEGF165 or FGF-1, improves oxygenation in MCF-7 breast tumours |
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